In the United States alone, hemorrhagic shock kills about 50,000 people each year
Is permissive hypotension due to fear of adverse effects of vasopressors, (which were initially thought to be harmful, in trauma patients) the only sensible treatment?
However, it should be borne in mind that prolonged (secondary to hypotension) hypoperfusion puts the patient at risk of developing multiple organ failure and death.
23 peer-reviewed studies
During the late phase of hypovolemic shock, hypotension results from a decrease in the activity of the sympathetic nervous system and a shift to a phase of “sympathetic inhibition,” and although the production of epinephrine and norepinephrine increases, as well as other substances attempting to counteract constant blood loss, such as angiotensin II and vasopressin, even a supply of whole blood may not restore normal blood pressure. In addition, there is endothelial damage, inflammatory response in the course of secretion from damaged cells – DAMP (damage-associated molecular patterns), coagulopathy which leads to irreversible changes resulting in hypoperfusion, acidosis and ……
The first data on the use of vasopressors in trauma spoke of increased mortality sometimes as much as 11 times higher than in the group without vasopressors (43.6% vs. 4.2%).
Newer data (2018) from Japan – 298 patients – patients who received vasopressors within 24 hours of admission vs. patients who did not. Vasopressor group = higher mortality rate.
HOWEVER, THERE ARE STILL NO CLEAR DATA ON TARGET OPTIMAL ARTERIAL PRESSURE IN RESUSCITATION OF PATIENTS WITH HEMORRHAGIC SHOCK or the data are from poor quality studies
However, there are reports that the supply of vasopressin, in addition to increasing pressure, also leads to support of hemostasis (the need for less blood transfusion) and even an anti-edematous effect in head trauma (hyperosmolar therapy has been used less frequently).