Brain parenchyma PO sub 2, PCO sub 2, and pH during and after hypoxic, ischemic brain insult in dogs
OBJECTIVES 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult. DESIGN Prospective...
Gespeichert in:
Veröffentlicht in: | Critical care medicine 1996-11, Vol.24 (11), p.1858-1868 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | OBJECTIVES 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult.
DESIGN Prospective, controlled, animal study in an acute experimental preparation.
SETTING Physiology laboratory in a university medical school.
SUBJECTS Fourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated.
INTERVENTIONS Anesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FIO2 0.21). Mechanical ventilation was established to maintain end-tidal PCO2 approximate 35 torr (approximate 4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FIO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximate 40 mm Hg produced with isoflurane approximate 4%). After 45 mins, carotid artery occlusion was released, FIO2 was reset to 0.21, and anesthetic was returned to halothane (approximate 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult.
MEASUREMENTS AND MAIN RESULTS Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximate 1-hr intervals.Baseline data agreed closely with other published resultsbrain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2 |
---|---|
ISSN: | 0090-3493 1530-0293 |
DOI: | 10.1097/00003246-199611000-00016 |