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Common arterial trunk
Medical expert of the article
Last reviewed: 07.07.2025
The common arterial trunk is formed if, during intrauterine development, the primitive trunk is not divided by a septum into the pulmonary artery and aorta, resulting in the formation of a single large arterial trunk, which is located above a large, perimembranous infundibular ventricular septal defect. Accordingly, mixed blood enters the systemic circulation, the lungs and the brain. Symptoms of the common arterial trunk include cyanosis, malnutrition, sweating, and tachypnea. A normal first heart sound and a loud single second heart sound are often heard; the murmur may vary. The diagnosis is based on echocardiography or cardiac catheterization. Medical treatment of heart failure is usually followed by surgical correction. Endocarditis prophylaxis is recommended.
The common arterial trunk accounts for 1-2% of congenital heart defects. About 35% of patients have DiGeorge syndrome or palatocardiofacial syndrome. There are 4 known types. In type I, the pulmonary artery branches off the trunk, then divides into the right and left pulmonary arteries. In types II and III, the right and left pulmonary arteries branch off independently from the posterior and lateral sections of the trunk, respectively. In type IV, arteries branching off the descending aorta supply the lungs; this type is currently considered a severe form of tetralogy of Fallot.
Other anomalies (eg, truncal valve insufficiency, coronary artery anomalies, atrioventricular communication, double aortic arch) may also be present and may increase postoperative mortality.
Physiologic sequelae of type I include mild cyanosis, heart failure (HF), and markedly increased pulmonary blood flow. In types II and III, cyanosis is more noticeable and HF is rare because pulmonary blood flow is normal or only slightly increased.
[ Symptoms of the common arterial trunk
In neonates with type I, manifestations include mild cyanosis and symptoms and manifestations of heart failure (tachypnea, malnutrition, sweating), which appear in the first weeks of life. Neonates with types II and III have more pronounced cyanosis, but heart failure develops less frequently.
Physical examination may reveal an increased cardiac impulse, increased pulse pressure, a loud and single 2nd heart sound, and an ejection click. A holosystolic murmur of intensity 2-4/6 is heard along the left edge of the sternum. A mitral valve murmur in mid-diastole may be heard at the apex with increased blood flow in the pulmonary circulation. With insufficiency of the arterial trunk valve, a high-pitched, decreasing diastolic murmur is heard in the 3rd intercostal space to the left of the sternum.
Diagnostics of the common arterial trunk
The diagnosis is suggested by clinical data, taking into account chest X-ray and ECG, and the exact diagnosis is established by two-dimensional echocardiography with color Doppler. Cardiac catheterization is often necessary to clarify associated anomalies before surgery.
Chest radiography shows cardiomegaly of varying degrees with increased pulmonary markings, a right aortic arch (in about 30%), and relatively high pulmonary arteries. ECG often shows hypertrophy of both ventricles. Significant increases in pulmonary blood flow may cause signs and symptoms of left atrial hypertrophy.
Treatment of the common arterial trunk
Heart failure is treated with aggressive drug therapy, including diuretics, digoxin, and ACE inhibitors, followed by early surgery. Intravenous prostaglandin infusion has no significant benefit.
Surgical treatment of the common arterial trunk consists of complete primary correction of the defect. The interventricular septal defect is closed so that blood flows into the arterial trunk from the left ventricle. A channel with or without a valve is placed between the right ventricle and the origin of the pulmonary arteries. Surgical mortality is 10-30%.
All patients with truncus arteriosus should receive endocarditis prophylaxis before dental or surgical procedures that may result in bacteremia.