Introduction:

Persistent truncus arteriosus is a rare congenital cardiac malformation that causes various complications in the cardiovascular system. It is characterized by the presence of a defective ventricular septum, a single truncal valve and a common truncus arteriosus between the pulmonary artery and aorta, leading to a mixture between arterial and venous blood, due to a predominantly left-to-right bidirectional cardiac shunt that compromises the supply of blood flow, nutrients, and systemic oxygenation. Clinical manifestations include desaturation with cyanosis, hypoxemia, tachycardia, tachypnea, alterations in cardiac contractility, abnormal distal pulses, weight loss, fatigue, and hepatomegaly.

Aim:

The purpose of this research is to establish hypotheses about the various compensatory mechanisms that are activated at a systemic level to counteract the effects of this malformation.

Reflection:

It is suggested that similar biomolecular responses occur in the cardiovascular, pulmonary, and renal systems, reducing nitric oxide production and causing vasoconstrictive responses. At the liver level, growth factors are generated and angiogenesis processes are initiated to increase blood perfusion. In the brain, enzymes are activated to increase blood flow and provide oxygen and essential nutrients.

Conclusion:

Despite these compensatory mechanisms, they fail to completely counteract the clinical manifestations, leading to a series of health problems such as pulmonary hypertension, heart failure, hepatomegaly, organ hypoperfusion, and neurological deficits. These factors converge to generate a complex cardiac condition that triggers adaptive responses in the body that end up being a challenging and potentially serious medical condition.

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