S. Strebel

Effects of the Valsalva Maneuver on Cerebral Circulation in Healthy Adults: A Transcranial Doppler Study

BACKGROUND AND PURPOSE Knowledge is limited about the effects of the Valsalva maneuver on cerebral circulation because of the poor temporal resolution of traditional cerebral blood flow measurements. The purpose of this study was to investigate changes in cerebral blood flow during the Valsalva maneuver and to explore its potential use for the evaluation of cerebral autoregulation. METHODS Using transcranial Doppler ultrasonography, we simultaneously recorded systemic arterial blood pressure in the radial artery and flow velocities in both middle cerebral arteries in 10 healthy adults during the Valsalva maneuver. Goslings pulsatility index was calculated for all phases of the Valsalva maneuver. Autoregulatory capacities were estimated from the change in cerebrovascular resistance (flow velocity in relationship to blood pressure) during phase II and changes in the velocity-pressure relationship in phase IV relative to phase I. RESULTS The characteristic changes in blood pressure (phases I to IV) were seen in all subjects, accompanying distinct changes in cerebral blood flow velocity. The relative changes in mean velocity during phases II and IV were significantly greater than those in mean blood pressure. Compared with the baseline value, velocity decreased by 35% in phase IIa, then rose by 56.5% in phase IV (corresponding changes in blood pressure were -10.2% and +29.8%, respectively). During phase II, the pulsatility and cerebrovascular resistance decreased by 19.9%. The increase in cerebral blood flow velocity in phase IV was significantly higher than in phase I (P < .0004), and there was no corresponding significant difference in blood pressure. CONCLUSIONS These results demonstrated that in healthy humans the Valsalva maneuver causes characteristic changes in systemic blood pressure as well as in flow velocity in the middle cerebral artery, reflecting the sympathetic and cerebral autoregulatory responses, respectively. Analysis of these changes may provide an estimate of autoregulatory capacity.

Impaired cerebral autoregulation after mild brain injury

BACKGROUND Severe head injury may impair cerebral autoregulation, which can increase the risk of secondary neuronal injury. The likelihood of impairment in autoregulation is assumed to be low with mild head injury. We report here the absence of cerebral autoregulation in a patient who suffered a concussion from an automobile accident 6 days earlier. METHODS The patient participated in a clinical study approved by the institutional human subjects review committee, investigating the dose-effect relationship of anesthetics on cerebral autoregulation. The patient was scheduled to undergo repair of a knee injury suffered during a motor vehicle accident, during which she had a concussion. The screening evaluation revealed no evidence of neurologic disease. The test was to be performed three times in each patient: baseline autoregulation measurements during stable fentanyl-nitrous oxide anesthesia, second and third measurements during low dose and high dose of the anesthetic to which the patient was assigned. Autoregulation was tested by increasing the mean systemic blood pressure from 80 mm Hg-100 mm Hg using a phenylephrine infusion while simultaneously recording flow velocity from a middle cerebral artery using transcranial Doppler ultrasonography. RESULTS Static autoregulation testing during baseline testing demonstrated complete absence of this homeostatic mechanism and the study was canceled. Repeated testing in the recovery unit after the patient awoke showed identical results. CONCLUSIONS Trivial mild head injury may result in loss of cerebral autoregulation. A clinical study of a larger series to document the incidence is warranted.

Third degree heart block and asystole associated with spinal anesthesia

CARDIAC arrest is a well-established complication of spinal anesthesia. 1-7 We present a case of spinal anesthesia-induced asystole in which onset and recovery could be recorded by means of Holter monitoring. Holter monitoring revealed that shortly after subarachnoid injection, a first degree heart block developed that, without any previous change in heart rate, progressed to a complete heart block. After successful resuscitation, a first degree heart block that persisted until 6 h after subarachnoid injection partly outlasted sensory and motor blockade.

Effect of the Valsalva Maneuver on Intracranial Hypertension

We describe a case of intracranial hypertension in a previously healthy 25-year-old man who sustained a head injury in a motor vehicle accident, in whom a Valsalva maneuver resulted in parallel reductions in mean arterial blood pressure, cerebral blood flow velocity in the middle cerebral artery, and intracranial pressure. The effects of raising intrathoracic pressure in patients with intracranial hypertension are discussed.

Dynamic and Static Cerebral Autoregulation during Isoflurane, Desflurane, and Propofol Anesthesia

Background Although inhalation anesthetic agents are thought to impair cerebral autoregulation more than intravenous agents, there are few controlled studies in humans.

Cerebrovascular Response lo Carbon Dioxide During Sodium Nitroprusside- and Isoflurane-Induced Hypotension

We have examined the cerebrovascular response to carbon dioxide during normotension, sodium nitroprusside (SNP)-induced hypotension and high dose isoflurane-induced hypotension in 10 patients who received a standardized general anaesthetic. Carbon dioxide reactivity was determined by varying PaCO2 between 3.0 and 8.0 kPa and recording simultaneously blood flow velocity from the middle cerebral artery (vmca). The paired vmca-PaCO2 data were analysed using linear regression to determine carbon dioxide reactivity. During hypotension, both high-dose isoflurane and SNP reduced significantly mean absolute (from 17.4 (SEM 2.3) to 13.0 (1.7) and 8.8 (1.3) cm s-1 kPa-1, respectively; P < 0.05) and relative (from 32.5 (3.8) to 23.6 (2.0) and 15.5 (1.3)% kPa-1, respectively; P < 0.05) cerebrovascular reactivity to carbon dioxide. This reduction was greater during SNP-induced hypotension (P < 0.05). We conclude that cerebrovascular reactivity to carbon dioxide was attenuated during isoflurane and SNP-induced hypotension, and that it was better preserved during isoflurane-induced hypotension.