Cerebral perfusion pressure directed therapy following traumatic brain injury and hypotension in swine.
There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S(cv)O(2)), cerebro-vascular carbon dioxide reactivity (DeltaS(cv)O(2)), and brain structural damage (beta-amyloid precursor protein [betaAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 +/- 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better S(cv)O(2) (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO(2) evoked a 16 +/- 4% increase in S(cv)O(2), indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in betaAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO(2) reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
Malhotra
Ajai K
AK
Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, 1200 E. Broad Street, West Hospital, 15th Floor East, PO Box 980454, Richmond, VA 23298, USA. akmalhot@hsc.vcu.edu
Schweitzer
John B
JB
Fox
Jerry L
JL
Fabian
Timothy C
TC
Proctor
Kenneth G
KG
D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D007022:Hypotension / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D007427:Intracranial Pressure / Q000187:drug effects / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology / Q000627:therapeutic use*; D013552:Swine
D010656:Phenylephrine