Objectives: The aims of the present study were to describe the temporal hemodynamic and oxygen transport patterns of patients with head injuries as well as the patterns of those who became brain dead to better understand the role of underlying central regulatory hemodynamic mechanisms and ultimately to improve rates of organ donation.
Methods: We studied 388 consecutive noninvasively monitored patients with severe head trauma; 79 of these became brain dead. Monitoring was started shortly after admission to the emergency department and was designed to describe the sequence of cardiac, pulmonary, and tissue perfusion functions by cardiac index (CI), mean arterial pressure, heart rate, arterial saturation by pulse oximetry (Sapo2), and transcutaneous oxygen and carbon dioxide (Ptco2/Fio2 and Ptcco2) patterns. The latter were used as markers of tissue perfusion or oxygenation.
Results: Patients with head injuries who subsequently became brain dead initially had low CI with poor tissue perfusion beginning shortly after emergency department admission. This was followed by a prolonged period characterized by high CI (4.43 ± 1.3 L · min-1 · m-2) and enhanced tissue oxygenation (Ptco2/Fio2 238 ± 186). In the late or end stage of brain death, hemodynamic deterioration and collapse led rapidly to arrest. In attempts to maintain hemodynamic stability for organ donation, the effects of various therapies on the hemodynamic patterns were preliminarily described.
Conclusions: The hyperdynamic state with exaggerated peripheral tissue perfusion or oxygenation in brain-dead patients associated with loss of central vasoconstrictive mechanisms of the stress response resulted in unopposed peripheral metabolic vasodilatation producing high CI and tissue perfusion.