ABSTRACT
The brachial plexus was identified by electrical stimulation before interscalene block with 30 mL 0.5% bupivacaine and adrenaline 1:200,000. During injection, compression was applied with a finger proximal to the injection site. Spirometric measurements were made before the block, and then at 5 min, 10 min, 20 min and 4 h after the injection. Diaphragmatic excursion was measured radiographically before the block, and at 15 min and 4 h afterwards. In 25 patients studied, spirometric measurements decreased. Twenty minutes after the injection, the forced vital capacity was 27% less, forced expiratory volume at 1 s 34% less and peak expiratory flow rate 15% less (all P < 0.05). Right diaphragmatic excursion decreased from 4.5 cm (SD 1.2 cm) to 1.8 cm (0.6 cm) at 15 mins and to 1.1 cm (0.6 cm) at 4 h (P < 0.05). Identification of the plexus by electric stimulation combined with finger compression above the injection site did not prevent diaphragmatic paresis.
Subject(s)
Anesthetics, Local/administration & dosage , Brachial Plexus , Bupivacaine/administration & dosage , Neck Muscles/innervation , Nerve Block , Phrenic Nerve/drug effects , Adrenergic Agonists/administration & dosage , Adult , Aged , Anesthetics, Local/adverse effects , Brachial Plexus/physiology , Bupivacaine/adverse effects , Diaphragm/diagnostic imaging , Diaphragm/drug effects , Electric Stimulation , Epinephrine/administration & dosage , Female , Follow-Up Studies , Forced Expiratory Volume/drug effects , Humans , Injections, Intramuscular , Male , Middle Aged , Nerve Block/adverse effects , Peak Expiratory Flow Rate/drug effects , Pressure , Radiography , Respiratory Paralysis/chemically induced , Spirometry , Vital Capacity/drug effectsABSTRACT
We have compared cardiorespiratory variables in anaesthetized piglets whose lungs were ventilated with oxygen in nitrous oxide (N2O group) or nitrogen (N group) after right ventricular carbon dioxide boluses (0.5 or 1 ml kg-1; n = 12) or slow graded injections (n = 6). Boluses affected all variables studied significantly (P < 0.05) except mean systolic arterial pressure. Significant changes in PE'CO2 (P = 0.012) and PaO2 (P = 0.048) values were observed in the N2O group. Changes in PaCO2 were related to volumes of injected carbon dioxide (P = 0.044). Boluses of 1.0 ml kg-1 induced severe circulatory collapse in two piglets in the N2O group. Slow embolization altered respiratory variables significantly (P < 0.001)). PaO2 decreased significantly in the N2O group (P < 0.0001). Mean pulmonary arterial pressure increased significantly over time (P = 0.001) and lasted longer in the N2O group (P < 0.05). Volumes and time required to induce a 50% increase in mean pulmonary arterial pressure differed significantly between groups (P < 0.05). We conclude that nitrous oxide worsened the effects of rapid and slow carbon dioxide emboli on cardiopulmonary variables. Rapid carbon dioxide embolism altered respiratory and haemodynamic variables, while slow carbon dioxide embolism changed only respiratory variables.
Subject(s)
Anesthesia, General , Anesthetics, Inhalation/adverse effects , Carbon Dioxide/adverse effects , Embolism, Air/chemically induced , Nitrous Oxide/adverse effects , Anesthetics, Inhalation/pharmacokinetics , Animals , Carbon Dioxide/pharmacokinetics , Carbon Dioxide/physiology , Drug Synergism , Embolism, Air/metabolism , Female , Hemodynamics/drug effects , Male , Nitrous Oxide/pharmacokinetics , Oxygen/physiology , Partial Pressure , Pulmonary Gas Exchange/drug effects , SwineSubject(s)
Anesthesia, Spinal/adverse effects , Cochlear Diseases/etiology , Vestibular Diseases/etiology , Cochlear Diseases/diagnosis , Diagnosis, Differential , Hearing Loss, Sensorineural/etiology , Humans , Male , Meniere Disease/diagnosis , Middle Aged , Vertigo/etiology , Vestibular Diseases/diagnosisABSTRACT
Cardiorespiratory changes induced by pneumoperitoneum and head-up tilt may generate alveolar ventilation to perfusion ratio changes and increased systemic vascular resistances. The reliability of end-tidal carbon dioxide tension and pulse oximetry in predicting arterial carbon dioxide partial pressure and arterial oxygen saturation may therefore be affected. The 35 ASA 1-2 patients in this study comprised 12 men and 23 women aged 48 (SD 17) years and weighing 71 (SD 14) kg. Twenty-nine were to undergo upper abdominal laparoscopy for cholecystectomy and six hyperselective vagotomy. Intra-abdominal pressure was 1.7 (SD 0.9) kPa and head-up tilt was 5.6 (SD 4.2) degrees. After abdominal insuflation, arterial carbon dioxide partial pressure significantly increased (p < 0.05). However, the arterial carbon dioxide partial pressure-end-tidal carbon dioxide partial pressure gradient remained constant throughout surgery. This gradient was highly correlated with arterial carbon dioxide partial pressure (p < 0.0001), but was not correlated with elapsed time, intra-abdominal pressure or head-up tilt. Arterial oxygen saturation was always greater than 95% in all patients and the arterial oxygen saturation-pulse oximetric saturation gradient was always less than or equal to +4%. In conclusion, end-tidal carbon dioxide partial pressure and pulse oximetric saturation allow reliable monitoring of arterial carbon dioxide partial pressure and arterial oxygen saturation in the absence of pre-existing cardiopulmonary disease and/or acute peroperative disturbance.
