Cerebral hemodynamic crisis. Physiology, pathophysiology, and approach to therapy.
The physiology and pathophysiology of the cerebral circulation have been discussed in relation to treatment of the cerebral hemodynamic crisis. Data are presented to show how cerebral vascular resistance, the intracranial compartments, and brain metabolic demand may be manipulated to effect internal decompression and raise local perfusion pressures. It is quite apparent that irreversibility occurs rapidly in cases of complete ischemia and therapeutic success is often limited by this fact. Application of sound therapeutic principles will limit the extent of cellular destruction. Of particular importance to the general surgeon treating the multiply injured patient, is the effect of anesthesia on intracranial pressure in patients with compromised intracranial volume reserve.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000768:Anesthesia, General; D001930:Brain Injuries / Q000601:surgery; D001932:Brain Neoplasms / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics; D006706:Homeostasis; D007036:Hypothermia, Induced; D000860:Hypoxia / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000503:physiopathology; D007427:Intracranial Pressure; D008833:Microcirculation / Q000503:physiopathology; D011559:Pseudotumor Cerebri / Q000503:physiopathology
D000305:Adrenal Cortex Hormones