Oxygen consumption and delivery relationship in brain-dead organ donors.

The oxygen delivery (DO2) and consumption (VO2) relationship in brain-dead organ donors is unknown. Therefore, in a prospective study, we determined the DO2/VO2 relationship in 21 consecutive brain-dead patients. Patients were allocated to one of two groups, according to plasma lactate concentration: normal (group NL, n = 11) or high (> 2.5 mmol litre-1) (group HL, n = 10). VO2 was measured independently, using indirect calorimetry, under control conditions, during low DO2 challenge with PEEP administration, and high DO2 challenge with inflation of medical antishock trousers and volume expansion or blood transfusion, as required. Under control conditions, there were no significant differences between groups NL and HL in haemodynamic or oxygenation variables, both groups having a low VO2 (mean 114 (SD 21) ml min-1 m-2). In group HL there was a different DO2/VO2 relationship pattern, with a dependent VO2 only. The mean slope of the DO2/VO2 relationship was significantly higher in group HL than in group NL (0.12 (0.09) vs 0.04 (0.07), P < 0.05). We conclude that brain death was associated with a low VO2, and patients in group HL exhibited DO2/VO2 dependency which was not observed in patients in group NL.

Inferences about respiratory muscle use after cardiac surgery from compartmental volume and pressure measurements.

BACKGROUND: After upper abdominal surgery, patients have been observed to have alterations in respiratory movements of the rib cage and abdomen and respiratory shifts in pleural and abdominal pressure that suggest dysfunction of the diaphragm. The validity of making such deductions about diaphragm function from these observations is open to discussion. METHODS: In eight adult patients, American Society of Anesthesiologists physical status 2, scheduled for elective cardiac surgery, we measured respiratory rate, tidal volume, rib cage and abdominal cross-section changes, and esophageal (Pes) and gastric (Pga) pressures preoperatively, 1 day postoperatively, and 5 days postoperatively. These data were analyzed in detail by following the variables through each respiratory cycle. RESULTS: Mean delta Pga/delta Pes decreased from 0.73 preoperatively to -0.56 1 day postoperatively and recovered to 0.47 5 days postoperatively. Plots of Pes against Pga and rib cage against abdominal expansion (Konno-Mead diagrams) were constructed. Six patients showed a postoperative pattern of breathing similar to that seen in patients who have undergone abdominal surgery: a decrease in the ratio of delta Pga/delta Pes and a shift toward rib cage expansion, with an increase in breathing rate and a decrease in tidal volume. This change was accomplished in most cases by the use of abdominal muscles in expiration with an increase in inspiratory intercostal muscle action without an increase in diaphragm activation, that is, a shift in the normal balance of respiratory muscle use in favor of muscles other than the diaphragm. A different ventilatory pattern was observed in the other two patients, consisting of minimal rib cage excursion and a large abdominal excursion. In these cases tidal volume was generated largely by contraction and relaxation of abdominal muscles with probable reduction in diaphragm activity. In addition, five patients exhibited positive changes in Pes at the end of inspiration that corresponded to closure of the upper airway, relaxation of inspiratory muscles, and subsequent opening of the airway with sudden exhalation, producing a grunt. CONCLUSIONS: Indirect measurements of respiratory muscle action based on pressure and chest wall motion are easier than are assessments based on implanted electromyogram electrodes and sonomicrometers that measure electric activity and muscle length, respectively, directly. Interpretation requires numerous assumptions and detailed analysis of phase relations among the variables. In patients after thoracic surgery, however, these measurements strongly point to a shift in the distribution of motor output toward muscles other than the diaphragm.

Effects of thoracic extradural block on diaphragmatic electrical activity and contractility after upper abdominal surgery.

BACKGROUND: Upper abdominal surgery (UAS) induces diaphragmatic dysfunction. Thoracic extradural block (TEB) using 0.5% bupivacaine improves some pressure and motion indices of diaphragmatic function. However, no direct information on diaphragmatic activity is available after UAS. The aim of this study was to assess diaphragmatic electrical activity (Edi) after UAS before and after TEB. METHODS: A postoperative electromyogram was obtained, using intramuscular electrodes inserted by the surgeon in the costal and crural parts of the diaphragm, in 14 patients undergoing abdominal aortic surgery. Tidal changes in abdominal (VAB) and rib-cage (VRC) volumes, and gastric (delta Pgas), esophageal (delta Pes), and transdiaphragmatic (delta Pdi) pressures were used to measure tidal volume (VT) and respiratory rate and to provide indirect indices of diaphragmatic activity from the two ratios VAB/VT and delta Pgas/delta Pdi. These respiratory variables were obtained preoperatively. Postoperatively, measurements including Edi were obtained before and after a segmental epidural block, reaching a T4 level was achieved with 0.5% plain bupivacaine. RESULTS: Upper abdominal surgery induced an increase in respiratory rate (+28 +/- 15%; P < .01), associated with a decrease in VAB/VT (from 0.75 +/- 0.11 to 0.07 +/- 0.08; P < .01), delta Pgas/delta Pdi (from 0.3 +/- 0.08 to 0.01 +/- 0.19; P < .05), and VT (-30 +/- 14%; P < .01). After surgery, all patients exhibited electrical diaphragmatic activity that increased with TEB by 48 +/- 28% (P < .01) and 60 +/- 22% (P < .001) for the cural and costal segments, respectively. The ratio delta Pdi/Edi, used to evaluate diaphragmatic contractility, was not modified by TEB. Tidal volume, respiratory rate, and delta Pgas/delta Pdi returned to preoperative levels, whereas VAB/VT increased but remained different from preoperative values. CONCLUSIONS: This study demonstrates that TEB produces an increase in diaphragmatic activity, identical for the two segments of the muscle. Interruption of afferents that produce an inhibitory effect on diaphragmatic activity appears the most attractive hypothesis to explain the consequences of TEB after UAS.

Variation in arterial to end-tidal CO2 tension differences during anesthesia in the "kidney rest" lateral decubitus position.

The course of arterial to end-tidal carbon dioxide tension difference [P(a-ET)CO2] was evaluated during general anesthesia in 25 patients scheduled for renal surgery performed in the "kidney position." The difference between arterial PCO2 (PaCO2) corrected to body temperature, and end-tidal PCO2 (PETCO2) measured by mass spectrometry was assessed after induction of anesthesia, after placement in the lateral decubitus position with back arched over a kidney bridge ("kidney position"), and every 20 min until the patients were replaced in the supine position at the end of the surgical procedure. Heart rate, arterial blood pressure, and esophageal temperature were simultaneously recorded. After induction of anesthesia, when the patients were lying supine (T1), P(a-ET)CO2 was 4.8 +/- 3.9 mm Hg (mean +/- SD). Placing the patients in the kidney position (T2) induced a significant increase in P(a-ET)CO2 (to 7.9 +/- 3.5 mm Hg; P less than 0.01). These alterations occurred without any significant change in mean arterial blood pressure or heart rate. A progressive increase in mean P(a-ET)CO2 occurred with maintenance of anesthesia; P(a-ET)CO2 reached 8.8 +/- 4.1 mm Hg (P less than 0.05 vs T2) and 8.9 +/- 4.4 mm Hg (P less than 0.05 vs T2) at 65 and 85 min, respectively, after lateral decubitus positioning. Large variations between and within patients were observed. Although stable mean arterial pressure was maintained, these changes were associated with a significant decrease in body temperature. These results demonstrate that P(a-ET)CO2 increases when patients are placed in the kidney position and may vary with the prolongation of anesthesia in this situation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory effects of medical antishock trousers in healthy volunteers.

The ventilatory effects of medical antishock trousers (MAST) were investigated using 10 healthy volunteers. Use of the MAST (60-80 mm Hg) decreased forced expiratory volume (-8% +/- 4%, p less than 0.01), vital capacity (-8% +/- 5%, p less than 0.01), and functional residual capacity (-12% +/- 6%, p less than 0.01) and induced a significant decrease in tidal volume (-30% +/- 17%, p less than 0.05), but minute ventilation was unmodified because of a concomitant increase in respiratory rate (+17% +/- 8%, p less than 0.001). The MAST modified the breathing pattern: the abdominal contribution to ventilation was markedly decreased (-57% +/- 22%, p less than 0.001), suggesting a decrease in the diaphragmatic contribution to ventilation. The MAST increased both the end-expiratory (+131% +/- 115%, p less than 0.01) and inspiratory variation (delta Pgas: +42% +/- 40%, p less than 0.05) of gastric pressure, whereas the end-expiratory and inspiratory variation of esophageal pressure remained unchanged. Because of a higher delta Pgas, the dynamic compliance of the abdominal compartment markedly fell (-77% +/- 10%, p less than 0.001). Transdiaphragmatic pressure (Pdi: +28% +/- 30%, p less than 0.05) significantly increased and the pressure-time index of the diaphragm significantly increased (+32% +/- 32%, p less than 0.05) after inflation of the MAST, suggesting an increase in the diaphragmatic cost of breathing. Inspiratory activity of the parasternal intercostal muscles significantly increased after the MAST was inflated. Computerized tomography showed that the MAST induced a cephalad shift of the diaphragm, which reduced pulmonary height.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of halothane on the electrical activity of respiratory muscles in rats]. / Effets de l'halothane sur l'activité électrique des muscles respiratoires du rat.

This study was designed to investigate the effects of halothane on the electrical activity of the respiratory muscles in rats. Indeed, halothane is known to reduce end-expiratory lung volume, both in man and in animal; this may be due to altered activity in the respiratory muscles. The electrical activity of the diaphragm, parasternal, intercostal and abdominal muscles were recorded using intramuscular electrodes in ten rats weighing between 400 and 450 g each. The rats were prepared under light halothane anaesthesia (tracheostomy, laparotomy, electrode positioning, plaster of Paris cast to impede leg movements). They were placed prone in a 20 1 plexiglass chamber, and allowed to awake. Thereafter halothane was vaporized in this chamber at a known concentration, until the animals no longer reacted to tail pinching. The measurements were carried out during the awake state, and under 2 vol % halothane. Muscle tone was assessed by the thickness of baseline inspiratory muscle activity at the end of expiration (maximally amplified raw electromyographic signals). The measurement of phasic electrical activity was carried out using peak inspiratory integrated electromyographic signals. Under halothane, phasic activity of the diaphragm was slightly reduced (p less than 0.05), whereas tonic activity remained unchanged. Parasternal intercostal muscle activity, both tonic and phasic, was also decreased during halothane anaesthesia (p less than 0.001). No phasic activity occurred in the abdominal muscles, but muscle tone was reduced during halothane administration (p less than 0.01). In rats, the decrease in intercostal muscle tone under halothane anaesthesia could play a major part in the fall in functional residual capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of an intubating dose of succinylcholine and atracurium on the diaphragm and the adductor pollicis muscle in humans.

This study compares the neuromuscular blocking effect of succinylcholine (0.8 mg . kg-1) and atracurium (0.6 mg.kg-1) on the diaphragm (D) and the adductor pollicis (AP) in 20 patients anesthetized with nitrous oxide, oxygen, and fentanyl. The diaphragm was monitored by measuring transdiaphragmatic pressure following bilateral phrenic nerve stimulation. After succinylcholine, the time from injection of succinylcholine to maximum depression of the single twitch response (onset time) was of 50 +/- 11 s (+/- SD) for D compared to 80 +/- 24 s for AP (P less than 0.001). After succinylcholine, recovery from paralysis was earlier for D than AP. Single twitch height (TH) returned to 25% of its control value (T25) after 5 +/- 2 min for D compared to 7 +/- 3 min for AP (P less than 0.001). Complete recovery of TH (T100) was achieved after 9 +/- 4 min for D and 11 +/- 5 min for AP (P less than 0.01). Recovery index (T25-75) was of 2 +/- 1 min for both muscles. After atracurium, the onset time for D was of 137 +/- 31 s compared to 181 +/- 45 s for AP (P less than 0.001). The T25 was achieved after 38 +/- 7 min for D compared to 63 +/- 13 min for AP (P less than 0.001). The TH of D returned to T100 after 60 +/- 12 min compared to 87 +/- 17 min for AP (P less than 0.01). The train-of-four ratio returned to 1 after 64 +/- 15 min for D compared to 99 +/- 21 min for AP (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)