Transcranial Doppler sonography and cerebrovascular CO₂-reactivity during whole body hyperthermia

Introduction

Disturbance of neurologic function is common in heat stroke patients. Loss of thermoregulatory response is associated with high mortality due to progressive brain edema. However, during whole body hyperthermia (WBH) for the treatment of metastatic cancer temperatures of above 41.8°C are intentionally applied [1]. Monitoring cerebral blood flow velocity therefore is a non-invasive method that may be useful in the detection of acute and potentially harmful alterations of the cerebral circulation.

Methods

After informed consent, in 10 ASA II patients with metastatic malignant disease who were eligible for WBH mean blood flow velocity (Vm) of the M1-segment of the middle cerebral artery was studied using a 2 MHz pulsed TCD device (TC 2-64, EME) with the probe fixed to the temporal window. The heating device was a RHS-7500 (Enthermics Medical Systems, USA). Target temperature was 41.8°C, time at target was 60 min. Anaesthesia was total intravenous anaesthesia by TCI using propofol (4-6 µg/kg/min). Patients were intubated and ventilated with an FiO₂ of 0.4 after induction with sufentanil (0.3-0.4 µg/kg), propofol and rocuronium (0.8 mg/kg). After induction of anaesthesia, three sequential measurements for Vm and Gosling's pulsatility index (PI) (systolic-diastolic/mean blood flow velocity) were taken during normo- and hypercapnia at baseline and at plateau and were averaged for each point of measurement. A two channel KEG was continuously recorded above the prefrontal cortex (Aspect Monitor A1000, Aspect Medical Systems). EEG data were processed online to yield bispectral index (BIS) values throughout the course of anaesthesia.

Results

During baseline, Vm at normocapnia (PaCO₂ 40.1 ± 0.99 mmHg) was 39.26 ± 11.81 cm/s. At hypercapnia (PaCO₂ 47.4 ± 2.08 mmHg), Vm was 55 ± 20.84 cm/s. CO₂ reactivity (?Vm/?PaCO₂) was 2.39 ± 0.9 cm/s/mmHg. During hyperthermia, Vm at normocapnia was 54.07 ± 21.19 cm/s, and almost doubled to 106.07 ± 40.43 cm/s at hypercapnia. CO₂ reactivity increased to 6.11 cm/s/mmHg. The PI under normocapnia significantly increased from 1.05 ± 0.2 (normothermia) to 1.49 ± 0.3 (hyperthermia). BIS readings remained below 35 during anaesthesia. During heating and plateau at 41.8°C an increase of cardiac index from baseline of up to 140% could he observed, which was due to a significant decrease of SVR and MAP. HR increased to 138 ± 27 bpm. None of the patients showed general or focal signs of CNS toxicity at 24 h after the treatment.

Discussion

During WBH under general anaesthesia a profound increase of cerebral blood flow velocity can be observed. This is partially due to the changes of systemic hemodynamic parameters, especially to increases of heart rate and cardiac index and to the decrease of MAP [2]. EEG data suggest that the observed effect is of primarily vascular origin and not due to increased CMRO2, although cerebral metabolism was not measured. Under WBH cerebrovascular reactivity was preserved and showed a marked positive dependency on baseline flow, as described previously [3]. Hyperventilation only slightly decreased Vm during hyperthermia, suggesting that patients with intracranial space-occupying lesions should be excluded from WBH treatment.