Teruo Kumazawa

Hypoxemia decreases the shivering threshold in rabbits anesthetized with 0.2 minimum alveolar anesthetic concentration isoflurane.

Shivering has been proposed as an etiology of postoperative hypoxemia.The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3[degree sign]C/h by perfusing water at 10[degree sign]C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7[degree sign]C at 130 mm Hg to 35.4[degree sign]C at 50 mm Hg (threshold = PaO2 [center dot] 0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold >1[degree sign]C. A 1[degree sign]C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia. Implications: Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia. (Anesth Analg 1998;87:1408-11)

Systemic, but not pulmonary, hemodynamics are depressed during combined high thoraco-cervical epidural and general anesthesia in dogs

PurposeAn epidural block is frequently combined with general anesthesia. Both systemic and pulmonary hemodynamics may be affected by high epidural anesthesia and the combined general anesthetic. These effects were investigated in a canine model.MethodsSystemic and pulmonary hemodynamics during a combined high thoraco-cervical epidural and general anesthesia were studied in dogs; the animals were anesthetized with propofol, 10 mg·kg−1·hr−1, or 2% sevoflurane, and then 1% mepivacaine, 5 mL, was injected epidurally between T1 and T2. Cardiac output (CO), pulmonary capillary wedge pressure (PCWP), pulmonary arterial pressure (PAP), mean arterial pressure (MAP), central venous pressure (CVP), electrocardiogram, and arterial and mixed venous gases were monitored for over 90 min after epidural mepivacaine. The interval between sevoflurane and propofol studies was two hours.ResultsBaseline measurement of MAP with sevoflurane anesthesia was significantly lower (P < 0.05-0.01) at every time point than with propofol anesthesia. After epidural mepivacaine (CI)-T7/8 blockade), MAP (P < 0.05-0.01), CO (P < 0.05-0.01), and heart rate (P < 0.05-0.01) decreased significantly during both propofol and sevoflurane anesthesia. In the sevoflurane group, stroke volume decreased significantly (P < 0.05-0.01) but recovered; however, MAP (P < 0.01) and CO (P < 0.05) did not recover 90 min after the injection. Mean CVP and systemic vascular resistance were not altered. There were no changes in mean PAP, mean PCWP, and pulmonary vascular resistance.ConclusionA combined high thoracic/general anesthesia depressed systemic hemodynamics, whereas the pulmonary circulation was not affected. The extent of the depression varied with the general anesthetics used, sevoflurane and propofol.RésuméObjectifUn bloc péndural est souvent combiné à l’anesthésie générale. L’hémodynamique générale et pulmonaire peut subir les effets de l’anesthésie péridurale haute et générale combinée. Ces effets ont été vérifiés chez un modèle canin.MéthodeL’hémodynamique générale et pulmonaire a été étudiée chez des chiens pendant une anesthésie péridurale haute thoraco-cervicale et générale combinée; les animaux ont été anesthésiés avec 10 mg·kg−1·hr−1 de propofol ou du sévoflurane à 2 %, suivi de mépivacaïne à 1 % donnée par injection péridurale entre T1 et T2. Le débit cardiaque (DC), la pression capillaire pulmonaire bloquée (PCPB), la tension artérielle pulmonaire (TAP), la tension artérielle moyenne (TAM), la pression veineuse centrale (PVC), l’électrocardiogramme et la gazométrie artérielle et du sang veineux mêlé ont été surveillés pendant 90 min après l’administration péridurale de mépivacaïne. Les données sur le sévoflurane et le propofol ont été prises à deux heures d’intervalle.RésultatsPour tous les temps de mesure, la TAM de base avec le sévoflurane a été significativement plus basse (P < 0,05-0,01) qu’avec le propofol. Après la mépivacaine péridurale (bloc CT-T7/8), la TAM (P < 0,05-0,01), le DC (P < 0,05-0,01) et la fréquence cardiaque (P < 0,05-0,01) ont baissé significativement pendant l’anesthésie au propofol ou au sévoflurane. Dans le groupe sévoflurane, le volume d’éjection a diminué de façon significative (P < 0,05-0,01) mais s’est rétabli; cependant, la TAM (P < 0,01) et le DC (P < 0,05) ne sont pas rétablies 90 min après l’injection. La PVC moyenne et la résistance vasculaire générale n’ont pas été touchées. Il n’y a pas eu de modification de la TAP, de la PCPB moyenne ou de la résistance vasculaire pulmonaire.ConclusionUne anesthésie thoracique haute et générale combinée déprime l’hémodynamique générale, mais la circulation pulmonaire n’est pas affectée. L’étendue de la dépression varie selon l’anesthésique utilisé, le sévoflurane ou le propofol.

Baroreflex sensitivity and hemodynamic changes in elderly and young patients during propofol anesthesia

young patients, aged 20–40 years (group Y) scheduled for elective surgery under general anesthesia participated in the present study. Patients with respiratory or cardiovascular disease, diabetes mellitus, or autonomic disorders, as well as patients receiving medication that affects cardiovascular function, were excluded. Premedication consisted of midazolam 0.05 mg·kg 1 administered intramuscularly 30min before anesthesia. Monitors were placed to measure, noninvasively, blood pressure, continuous electrocardiography, and pulse oximetry. A venous catheter was inserted, and acetated Ringer’s solution was infused at a rate of 10ml·kg 1·h 1. After measurements of blood pressure and heart rate, all patients were anesthetized with a bolus propofol injection (1.5 mg·kg 1), followed by continuous intravenous infusion (10 mg·kg 1·h 1). Vecuronium (0.15 mg·kg 1) was given, and tracheal intubation was performed. Ten min after intubation, blood pressure and heart rate were re-evaluated. Then phenylephrine (2 μg·kg 1) was injected. Blood pressure was measured by continuous mode, and heart rate was measured continuously for 10 min after the injection. Values for maximum increase in mean arterial blood pressure (∆MAP) and maximum reflex decrease in heart rate (∆HR) in response to phenylephrine-induced hypertension were obtained. The BRS was assessed as the ratio of ∆HR to ∆MAP (∆HR/∆MAP). Patients’ age, height, weight, and changes in blood pressure, changes in heart rate, and BRS were compared using unpaired t-test. Propofol-mediated changes in blood pressure and HR were analyzed by paired ttest. A P value less than 0.05 was considered statistically significant.