This study indicated that end-tidal PCO2 monitoring correlated well with PaCO2 in patients without respiratory complications or without spontaneous breathing, resulting in rebreathing of gases. However, its clinical validity is questionable in patients who have the greatest need for end-tidal PCO2 monitoring (i.e., patients who have respiratory distress or who are breathing spontaneously and overriding the ventilator.
BACKGROUND: Intracranial hypertension occurs in response to routine procedures such as endotracheal suctioning in patients with severe head injuries. In some patients, the intracranial pressure does not immediately return to baseline levels. OBJECTIVES: To examine the effect of drug administration on cerebrovascular response to endotracheal suctioning in adults with severe head injuries. METHODS: Seventy-one subjects were divided into 3 groups: those who received no drugs, those treated with opiates only (morphine sulfate and fentanyl citrate), and those treated with a neuromuscular blocking agent (vecuronium bromide) plus opiates. A controlled protocol involving 2 sequences of endotracheal suctioning that included hyperoxygenation, hyperinflation, and suctioning was used for all subjects. Two-way repeated-measures analyses of variance were done with type of drug as the between-subject factor and phase of suctioning as the within-subject factor. Survival analysis was used to compare the return of intracranial pressure to baseline levels among the 3 groups. RESULTS: Changes in intracranial pressure were significantly smaller in subjects who received a neuromuscular blocking agent plus opiates than in subjects who did not receive any drugs or received opiates only. The greatest increase in intracranial pressure from baseline was in the first and second phases of suctioning. The 3 groups showed no significant difference in the return of intracranial pressure to baseline level. CONCLUSIONS: Neuromuscular blockers attenuate the increases in intracranial pressure that occur with endotracheal suctioning. It is not known whether control of procedurally induced elevations in intracranial pressure affects long-term outcomes in adults with severe head injuries.
A repeated measures randomized within-group design was used to determine the effectiveness of controlled short-duration hyperventilation (HV) in blunting the increase of intracranial pressure (ICP) during endotracheal suctioning (ETS). A multimodal continuous real-time computerized data acquisition procedure was used to compare the effects of two HV ETS protocols on ICP, arterial pressure, cerebral perfusion pressure (CPP), heart rate, and arterial oxygen saturation in severe head-injured adult patients. The results indicated that short-duration HV for 1 minute, which decreases the PaCO2, reduced ETS-induced elevations in ICP while maintaining CPP. However, it is not clear whether short-duration HV is neuroprotective, particularly in ischemic regions of the brain. Therefore, before a change in practice is implemented on the use of short-duration HV as a prophylactic treatment against ETS-induced elevations in ICP, additional questions on cerebral oxygen delivery and uptake need to be answered.
Cerebrospinal fluid drainage is a first line treatment used to manage severely elevated intracranial pressure (> or = 20 mm Hg) and improve outcomes in patients with acute head injury. There is no consensus regarding the optimal method of cerebrospinal fluid removal. The purpose of this investigation was to determine whether cerebrospinal fluid drainage decreases intracranial pressure and improves cerebral perfusion and to identify factors that impact treatment effectiveness. This study involved 31 severely head injured patients. Intracranial pressure and other indices of cerebral perfusion (cerebral perfusion pressure, cerebral blood flow velocity, and regional cerebral oximetry) were measured before, during, and after cerebrospinal fluid drainage. Arterial and jugular venous oxygen content was measured before and after cerebrospinal fluid drainage. Patients underwent three randomly ordered cerebrospinal fluid drainage protocols that varied in the volume of cerebrospinal fluid removed (1 mL, 2 mL, and 3 mL) for a total of 6 mL of cerebrospinal fluid removed. There was a significant change in the intracranial pressure from a mean at baseline of 26.1 mm Hg (SD = 4.4) to 22.1 mm Hg immediately after drainage. One third of patients experienced a decrease in the intracranial pressure below 20 mm Hg; in two patients the intracranial pressure dropped less than 1 mm Hg. The following factors predicted 61.5% of the variance in the responsiveness of intracranial pressure to drainage: vecuronium hypothermia, baseline cerebral perfusion pressure and acuity of illness. Cerebrospinal fluid drainage provides a transient decrease in intracranial pressure without a measurable improvement in other indices of cerebral perfusion.
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