Resting energy expenditure in brain death.

OBJECTIVE: To evaluate resting energy expenditure (REE) in brain dead patients and to investigate the hypothesis that the reduction in REE results from a decrease in cerebral blood flow. DESIGN: Prospective, open labeled, control study. SETTING: General intensive care unit of a tertiary referral teaching hospital. PATIENTS: 30 critically ill patients with isolated head injury divided in two groups: group 1 patients (n = 10) with a Glasgow Coma Scale (GCS) score of 4 to 8 and group 2 patients (n = 20), in whom the final outcome was brain death (GCS = 3). Group 2 patients were divided into two subgroups: Group 2 a (n = 11) were admitted as brain dead (GCS = 3) and group 2 b (n = 9) were admitted with a GCS > 3 and progressed to brain death. INTERVENTIONS: Clinical and instrumental, using transcranial Doppler sonography (TCD), diagnosis of brain death. Cerebral blood flow studies of the middle cerebral artery bilaterally by bidimensional TCD and measurement of REE using indirect calorimetry. MEASUREMENTS AND RESULTS: Measurements of REE and TCD studies were performed simultaneously on admission and after hemodynamic and neurologic stabilization. In cases with progressive neurologic deterioration, serial measurements were performed REE values were expressed as percentage of basal metabolic rate (%BMR), which were estimated according to each patient's gender, age, height, and weight. Group 1 patients, had normal TCD patterns throughout their hospitalization and their REE value was 21 +/- 11 % higher than BMR. Group 2 patients demonstrated TCD patterns compatible with brain death and their REE value was 24.5 +/- 11 % lower than BMR (p < 0.01). Group 2 a patients, who were admitted as brain dead and remained brain dead, had REE values 30 +/- 11 % lower than BMR (p < 0.01). Group 2 b patients, who were not brain dead on admission but progressed to brain death, in serial measurements revealed a significant relationship between REE and TCD findings (R = -0.77, p < 0.0001). In this subgroup of patients, with multiple regression analysis a significant relationship was found only between REE and the TCD pattern, but not with body temperature. CONCLUSIONS: In brain dead patients, REE decreases to values lower than BMR. This can be attributed to the cessation of cerebral blood flow and consequently cerebral metabolism and not to hypothermia.

Ventilatory post-stimulus potentiation in patients with brain damage.

In normal humans when a brief hypoxic ventilatory stimulus is terminated abruptly by breathing 100% O2, ventilation during hyperoxia gradually declines to baseline prehypoxic levels without an undershoot. This has been interpreted as evidence of decay of short-term potentiation (STP), a mechanism located in the brainstem and not dependent upon higher center inputs. STP decay may be important in preventing periodic breathing by damping ventilatory responses to cyclic stimuli. Patients with brain damage commonly have periodic breathing that may be caused partly by impairment of STP activation. To test this 12 tracheostomized patients with severe brain damage (Glasgow score 9.9 +/- 0.6) were studied. Breathing stability was estimated by at least 6 h of capnography and from these records apnea index (AI, episodes/hour) and cyclic changes of end-tidal CO2 (c-PETCO2, cycles/hour) were derived. STP activation was examined by brief exposure to hypoxia (45 s, end-tidal O2 = 50 mm Hg) followed by hyperoxia. Forty-four hypoxic-hyperoxic runs were analyzed and compared with 19 normoxic-hyperoxic trials. At the end of the hypoxia ventilation (VI) increased 39.5 +/- 5.8% and PETCO2 decreased 2.7 +/- 0.6 mm Hg to 91.5 +/- 2.2% of baseline value. When hypoxia was terminated abruptly by hyperoxia VI dropped immediately to 63.2 +/- 7.2% of baseline, remaining for 35 s significantly lower than the corresponding values acquired during hyperoxia after normoxia. After hypoxia, apneas occurred in 19 of 44 hyperoxic runs. There was a negative relationship between nadir hyperoxic ventilation after hypoxia and both AI and c-PETCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of continuous haemofiltration-related hypothermia on haemodynamic variables and gas exchange in septic patients.

OBJECTIVE: To investigate the influence of continuous haemofiltration (CHF) on haemodynamics, gas exchange and core temperature in critically ill septic patients with acute renal failure. PATIENTS AND METHODS: In 20 patients (17 male, 3 female) ultrafiltration rate, core temperature, gas exchange and haemodynamic variables were measured at regular intervals during the first 48 h of haemofiltration. Baseline data were compared to those obtained 30 min after initiating CHF and also to those during hypothermia (if observed). MAIN RESULTS: Haemodynamic variables remained remarkably constant throughout the study period. In patients with a relatively low ultrafiltration rate (855 +/- 278 ml/h) temperature did not change, while in patients with a high ultrafiltration rate (1468 +/- 293 ml/h) core temperature significantly decreased from 37.6 +/- 0.9 degrees C to 34.8 +/- 0.8 degrees C (p < 0.001). There was a statistically significant correlation between temperature decrease and ultrafiltration rate (r = -0.68, Y = 1.8-0.003 X, p < 0.01). Hypothermic patients also showed a mean decrease in VO2 from 141 +/- 22 ml/min/m2 to 112 +/- 22 ml/min/m2 (p < 0.01) with a concomitant increase in PaO2 from 103 +/- 37 mmHg to 140 +/- 42 mmHg (p < 0.001) and in PvO2 from 35 +/- 4 mmHg to 41 +/- 5 mmHg (p < 0.001). CONCLUSIONS: 1) Continuous haemofiltration does not cause significant alternations in haemodynamic variables. 2) Hypothermia frequently occurs in patients undergoing continuous haemofiltration with high ultrafiltration rates. These hypothermic patients show a reduction in VO2 leading to an increase in PvO2 and PaO2. This mild hypothermia in these circumstances has no evident deleterious effects.