ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:The peripheral chemoreceptors are responsible for the ventilatory response to hypoxia (acute hypoxic response) and for 30% of the normoxic hypercapnic ventilatory response. To quantify the effects of subanesthetic concentrations of halothane on the respiratory control system, in particular on the peripheral chemoreceptors, we studied the response of humans to carbon dioxide and oxygen at two subanesthetic concentrations of halothane.Methods:Square-wave changes in end-tidal carbon dioxide tension (7.5-11.3 mmHg) and step decreases in end-tidal oxygen tension (arterial hemoglobin oxygen saturation 82 ± 2%; duration of hypoxia 5 min) were performed in nine healthy male subjects during 0, 0.05 (HA-1), and 0.1 minimum alveolar concentration (HA-2) halothane. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and off-set.Results:Fifty-six carbon dioxide responses and 27 oxygen responses were obtained. The peripheral carbon dioxide sensitivities averaged to 0.76 ± 0.141·min-1· mmHg-1(control), 0.50 ± 0.12 1·min-1· mmHg-1(HA-1), and 0.30 ± 0.08 1·min-1·mmHg-1(HA-2; P < 0.01 vs. control). The central carbon dioxide sensitivity did not differ significantly among treatment groups (control, 1.47 ± 0.22 1· min-1· mmHg-1; HA-1, 1.41 ± 0.51 1·min-1mmHg-1; and HA-2, 1.23 ± 0.30 1·min-1·mmHg-1). The time constants of the central chemoreflex loop showed a large decrease during the administration of 0.1 minimum alveolar concentration halothane. The acute hypoxic response declined from 15.0 ± 3.9 1·min-1to 10.9 ± 2.9 1·min-1(HA-1) and 4.8 ± 1.4 1·min-1(HA-2; P < 0.01 vs. control and HA-1). All values are means ± SEM.Conclusions:The results show depression of the ventilatory responses to hypoxia and hypercapnia during inhalation of subanesthetic concentrations of halothane. The depression is attributed to a selective effect of halothane on the peripheral chemoreflex loop. The oxygen and carbon dioxide responses mediated by the peripheral chemoreceptors are affected proportionally. It is argued that the decrease in central time constants is caused by an effect of halothane on central neuronal dynamics.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:These experiments were designed to study the effect of 0.1 minimum alveolar concentration isoflurane on the hypoxic ventilatory response as measured by two common methods of hypoxic testing: when normocapnic hypoxia was induced abruptly and when it was induced gradually. We hypothesized that any disparity in results would be due to an isoflurane effect that was manifested differently in the two tests.Methods:After 20 min for uptake and equilibration of 0.1 minimum alveolar concentration end-tidal isoflurane or carrier gas in hyperoxia, isocapnic hypoxia was induced either abruptly over 60-80 s (“step” test) or gradually over 10 min (“ramp” test), followed by 20 min of isocapnic hypoxia at 45 mmHg end-tidal oxygen. Control of the hypoxic and isocapnic stimuli was accomplished accurately by a computer-controlled dynamic end-tidal forcing system. Eight subjects performed each test in the presence and absence of isoflurane.Results:For both step tests and ramp tests, 0.1 minimum alveolar concentration isoflurane had no effect on minute ventilation during the defined periods of hypoxia. With isoflurane, Δ &OV0312;E45, the acute change in ventilation from hyperoxia to hypoxia, was 97 ± 20% (mean ± SEM) of the control response for step tests and 100 ± 25% of the control response for ramp tests. The step tests produced significantly larger acute hypoxic responses than did the ramp tests, but by the end of 20 min of hypoxia, ventilation was similar for both tests.Conclusions:Neither method of hypoxic testing demonstrated the level of isoflurane effect reported by others. A comparison of the two methods of hypoxic testing suggests that ramp tests, as commonly performed, do not allow adequate time for full expression of the acute hypoxic ventilatory response. Step tests also better separated the opposing hypoxic effects of carotid body stimulation and central ventilatory depression.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:Atelectasis formation during anesthesia may be due to loss of respiratory muscle tone, in particular that of the diaphragm. This was tested by tensing the diaphragm by phrenic nerve stimulation (PNS) and observing the effect on atelectasis.Methods:Twelve patients (mean age 48 yr) without preexisting lung disease were studied during halothane anesthesia. PNS was executed with an external electrode on the right side of the neck. Chest dimensions and area of atelectasis were studied by computed tomography of the chest.Results:Right-sided PNS against an occluded airway at functional residual capacity reduced the atelectatic area in the right lung from 5.1 to 3.8 cm2. The atelectasis was reduced to 1.1 cm2after application of positive end-expiratory pressure (PEEP) of 10 cmH2O and large tidal volumes but increased to 2.5 cm2within 1 min after discontinuation of PEEP. Commencement of PNS immediately after PEEP prevented the atelectasis from increasing, the mean area being 0.9 cm2. In seven patients, in whom the trachea was intubated with a doublelumen endobronchial catheter the atelectatic area was smaller during PNS with an open airway than during positive pressure inflation of the lung with the same volume as inspired during PNS (3.5 and 5.2 cm2, respectively.Conclusions:The findings indicate that contracting the diaphragm in the anesthetized subject reduces the size of atelectasis.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:Nitric oxide (NO) inhalation selectively decreases pulmonary artery hypertension and improves arterial oxygenation in patients with the adult respiratory distress syndrome (ARDS). In this study of patients with severe ARDS, we sought to determine the effect of inhaled NO dose and time on pulmonary artery pressure and oxygen exchange and to determine which patients with ARDS are most likely to show this response.Methods:Thirteen patients with severe ARDS (hospital mortality 67%) inhaled 0-40 parts per million (ppm) NO. Seven of these patients continued to breathe 2-20 ppm NO for 2-27 days.Results:Inhaling 5-40 ppm NO decreased mean pulmonary artery pressure in a dose-related fashion (from 34 ± 7 to 30 ± 7 mmHg at 20 ppm NO). Systemic arterial pressure did not change. The ratio of arterial oxygen tension to inspired oxygen fraction increased (from 126 ± 36 to 149 ± 38 mmHg) and the venous admixture decreased (from 31.2 ± 5.5 to 28.2 ± 5.2%) without a clear dose-response effect. During prolonged NO inhalation, 2-20 ppm NO effectively reduced mean pulmonary artery pressure (38 ± 7 vs. 31 ± 6 mmHg) and increased arterial oxygen tension (79 ± 10 vs. 114 ± 27 mmHg) without evidence of tachyphylaxis. The decrease of pulmonary vascular resistance during NO inhalation correlated with the level of pulmonary vascular resistance without NO (r=-0.72). The reduction of venous admixture correlated with the level of venous admixture without NO (r=-0.78).Conclusions:Long-term NO inhalation at low concentrations selectively decreases mean pulmonary artery pressure and improves arterial oxygen tension in patients with ARDS. The selective pulmonary vasodilation effect is most pronounced in ARDS patients with the greatest degree of pulmonary vasoconstriction.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:The diagnosis of an acute malignant hyperthermia reaction by clinical criteria can be difficult because of the nonspecific nature and variable incidence of many of the clinical signs and laboratory findings. Development of a standardized means for estimating the qualitative likelihood of malignant hyperthermia in a given patient without the use of specialized diagnostic testing would be useful for patient management and would promote research into improved means for diagnosing this disease.Methods:Using the Delphi method and an international panel of 11 experts on malignant hyperthermia, a multifactor malignant hyperthermia clinical grading scale comprising standardized clinical diagnostic criteria was developed for classification of existing records and for application to new patients.Results:This scale ranks the qualitative likelihood that an adverse anesthetic event represents malignant hyperthermia (malignant hyperthermia event rank) and that, with further investigation of family history, an individual patient will be diagnosed as malignant hyperthermia susceptible (malignant hyperthermia susceptibility rank). The assigned rank represents a lower bound on the likelihood of malignant hyperthermia. The clinical grading scale requires the anesthesiologist to judge whether specific clinical signs are appropriate for the patient's medical condition, anesthetic technique, and surgical procedure.Conclusions:The malignant hyperthermia clinical grading scale is recommended for use as an aid to the objective definition of this disease. Its use may improve malignant hyperthermia research by allowing comparisons among well-defined groups of patients. This clinical grading system provides a new and comprehensive clinical case definition for the malignant hyperthermia syndrome.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:The range of core temperaturesnottriggering thermoregulatory responses (“interthreshold range”) remains to be determined in humans. Although the rates at which perioperative core temperatures vary typically range from 0.5 to 2°C/h, the thermoregulatory contribution of different core cooling rates also remains unknown. In addition, sweating in women is triggered at a slightly greater core temperature than in men. However, it is unknown whether the vasoconstriction and shivering thresholds are comparably greater in women, or if women tolerate a larger range of core temperatures without triggering thermoregulatory responses. Accordingly, the authors sought to (1) define the interthreshold range; (2) test the hypothesis that, at a constant skin temperature, the vasoconstriction and shivering thresholds are greater during rapid core cooling than during slowly induced hypothermia; and (3) compare the sweating, vasoconstriction, and shivering thresholds in men and women.Methods:Eight men and eight women participated. The men participated on 2 separate days; no anesthesia or sedatives were administered. On each day, they were cutaneously warmed until sweating was induced and then were cooled by a central venous infusion of cold fluid. The cooling rates were 0.7 ± 0.1°C/h on 1 day and 1.7 ± 0.4°C/h on the other, randomly ordered. Skin temperature was maintained near 36.7°C throughout each trial. The women were studied only once, in the follicular phase of their menstrual cycles, at the greater cooling rate.Results:The interthreshold range was ≈ 0.2 °C in both men and women, but all thermoregulatory response thresholds were ≈ 0.3°C higher in women. All thresholds were virtually identical during slow and fast core cooling.Conclusions:Our findings confirm the existence of an interthreshold range and document that its magnitude is small. They also demonstrate that the interthreshold range does not differ in men and women, but that women thermoregulate at a significantly higher temperature than do men. Typical clinical rates of core cooling do not alter thermoregulatory responses.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background:Although diphenhydramine is frequently used to treat pruritus and nausea in patients who have received neuraxial opioids, there are no data regarding its effect on ventilatory control. We conducted the current study to evaluate the effects of diphenhydramine on hypercapnic and hypoxic ventilatory control in healthy volunteers.Methods:First, we measured the steady-state ventilatory response to carbon dioxide during hyperoxia with an end-tidal carbon dioxide tension of 46 or 54 mmHg (alternate subjects) in eight healthy volunteers. We then determined the hypoxic ventilatory response during isocapnic rebreathing at the same carbon dioxide tension. After a 10-min recovery period, we repeated the steady-state and hypoxic ventilatory response measurements at the other carbon dioxide tension (54 or 46 mmHg). Ten minutes after subjects received diphenhydramine 0.7 mg·kg-1intravenously, we repeated this sequence of ventilatory measurements.Results:Under hyperoxic conditions (inspired oxygen fraction > 0.5) diphenhydramine did not affect the ventilatory resposnse to hypercapnia. Similarly, at an end-tidal carbon dioxide tension of 46 mmHg, neither the slope nor the position of the hypoxic ventilatory response curve changed significantly after diphenhydramine. However, at an end-tidal carbon dioxide tension of 54 mmHg, the slope of the hypoxic ventilatory response increased from 1.28 ± 0.33 to 2.13 ± 0.61 1·min-1· %Spo2-1(mean ± standard error), and &OV0312;Eat an arterial hemoglobin oxygen saturation of 90% increased from 31.2 ± 3.1 to 43.1 ± 5.4 1·min-1).Conclusions:We conclude that although it did not affect the ventilatory response to carbon dioxide during hyperoxia or the ventilatory response to hypoxia at an end-tidal carbon dioxide tension of 46 mmHg diphenhydramine augmented the hypoxic response under conditions of hypercapnia in our young healthy volunteers. Although these findings may help to explain the apparent safety of diphenhydramine, they may not be applicable to debilitated patients or those who have received systemic or neuraxial ventilatory depressants.

ISSN:0003-3022    

出版商:OVID    

年代:1994

数据来源: OVID