Alterações arteriais na reação anafilática por picada de abelha: uma abordagem clínica

Abstract

The anaphylactic reaction caused by a bee sting can result in significant arterial changes, affecting the body's circulatory dynamics and homeostasis. The toxin released by the bee is responsible for the action of proteins capable of provoking an intense immune response in sensitized individuals. This mechanism triggers an immediate allergic reaction, marked by the substantial release of inflammatory mediators such as histamine and leukotrienes into the bloodstream. The cardiovascular system is significantly influenced by these mediators. Histamine, for example, induces the dilation of blood vessels (vasodilation) and increases vascular permeability. This dilation of the vessels results in a decrease in peripheral vascular resistance, potentially causing a sudden decrease in blood pressure (hypotension). Increased permeability allows fluids to accumulate in the tissues, leading to edema and exacerbating feelings of shortness of breath and swelling in areas such as the throat and tongue. In addition, cardiac function and peripheral circulation can be impacted by an anaphylactic reaction. If not treated promptly, low blood pressure can decrease blood flow to essential organs, potentially resulting in anaphylactic shock. The cardiovascular response may also manifest as tachycardia (an elevated heart rate), which serves as a compensatory mechanism for the heart to maintain cardiac output despite the drop in blood pressure. Treatment of anaphylaxis requires immediate administration of epinephrine, a substance that functions as a vasoconstrictor, helping to reverse vasodilation and increase blood pressure. In addition, epinephrine decreases vascular permeability and relieves airway constriction. Additional management may include intravenous fluids, corticosteroids, and antihistamines to control the allergic reaction and prevent recurrence.