Acute Vascular Insufficiency and Fainting

Acute Vascular Insufficiency and Fainting

Vascular insufficiency in the circulatory system is predominantly an acutely developing pathology. Acute vascular insufficiency of the circulation (AVIC) manifests in several forms: fainting, vasomotor collapse, and shock. Essentially, it is a syndrome characterized by a reduced volume of circulating blood. The causes of AVIC are either related to the redistribution of circulating blood volume (in fainting and vasomotor collapse) or to rapid fluid loss (due to diarrhea, vomiting, hemorrhage, burns, or surgical operations) — referred to as hypovolemic AVIC.

The most critical pathogenetic mechanism of severe AVIC involves capillary permeability disturbances and dilation of the capillary network (seen in toxic, septic, and anaphylactic shocks). In response to a sharp decrease in blood volume, a protective mechanism of circulatory centralization is triggered. This mechanism aims to preserve the blood flow to the brain and heart by increasing venous return. Sympathetic stimulation leads to a significant constriction of the skin, muscle, splanchnic, and renal vessels, thereby increasing peripheral vascular resistance. Nevertheless, tissue hypoperfusion is detected very early in severe AVIC.


Fainting is a sudden, short-term loss of consciousness due to acute cerebral hypoxia. Causes of fainting include nervous stress and sudden pulse deceleration. In heart diseases, fainting occurs in individuals with aortic stenosis during physical exertion, as well as during brief ventricular fibrillation or severe bradycardia.

Vasomotor collapse occurs when there is a disturbance in vasomotor regulation (such as in orthostatic disorders). The mechanism of fainting involves a sudden reduction in blood flow to the brain. Patients turn pale, break out in a sweat, experience anxiety followed by lethargy, blood pressure drops, the pulse quickens, and its strength decreases. This is a mild form of AVIC. Treatment is often possible on an outpatient basis.

Management and Treatment

Monitoring the patient’s condition involves measuring heart rate and blood pressure. In prolonged cases, it is advisable to measure central venous pressure and skin temperature. Often, treatment involves simply changing the patient’s body position to increase blood flow to the brain. Patients are laid in a horizontal position with the legs elevated if possible.

To stimulate reflex actions, increasing fresh air supply is beneficial. Inhalation of ammonia vapor can also be helpful. For bradycardia, ephedrine administration is indicated. If there is no rapid improvement, cordiamine or camphor should be administered. The use of sympathomimetics is generally unnecessary. Cardiac glycosides are contraindicated.

In summary, acute vascular insufficiency and fainting are critical conditions that require prompt recognition and management. Understanding the underlying mechanisms and appropriate interventions can significantly improve patient outcomes in these emergency situations.