thiopental and Hypercapnia

Myotonia is defined as a persistent contraction of skeletal muscles after their stimulation. This contracture is not prevented or relieved by regional anaesthesia or muscle relaxants. The sensitivity to non-depolarizing muscle relaxants is usually normal. Suxamethonium, neostigmine, hypothermia, a rise in kalaemia should be avoided. There have been case reports of malignant hyperthermia in patients with myotonia congenita. Dystrophia myotonica is the second most frequent of the inherited muscle diseases, after Duchenne's dystrophy. The severity of the disease is due more to the muscular atrophy and the multiple organ involvement than to the abnormal contraction. Atrioventricular heart block and dysrhythmias are more common than heart failure. Prolonged apnoea and pneumonia are the main risks of anaesthesia. In severe cases, exists a restrictive respiratory insufficiency which is preceded by a fall in the maximum expiratory pressure. Dysphagias and inefficient coughing may occur early. An increased susceptibility to hypnotic drugs and opiates is a common feature. Spontaneous sleep apnoeas should be sought before anaesthesia, especially by using pulse oximetry. The anaesthetic implications are reemphasized.

Topics: Anesthesia; Contracture; Disease Susceptibility; Female; Humans; Hypercapnia; Male; Malignant Hyperthermia; Myotonia; Neostigmine; Neuromuscular Nondepolarizing Agents; Succinylcholine; Thiopental

Topics: Anesthetics; Arrhythmias, Cardiac; Catecholamines; Digitalis Glycosides; Electroshock; Heart Diseases; Humans; Hypercapnia; Hypertension; Hypothermia, Induced; Hypoxia; Intubation; Neostigmine; Potassium; Scopolamine; Succinylcholine; Surgical Procedures, Operative; Thiopental

We evaluated the effectiveness of intentional hypercapnia against hypotension after induction of anaesthesia with thiopental and isoflurane (TI) or propofol (P). For each group, 24 patients were anaesthetized with thiopental 4 mg kg(-1) (TI) or propofol 2 mg kg(-1) (P) for tracheal intubation and then lightly anaesthetized with isoflurane at 0.6% end-expiratory concentration (TI) or by 6 mg kg(-1) h(-1) infusion of propofol (P). In both anaesthesia groups, patients were randomly assigned to either normocapnia (end-tidal CO(2) = 35 mmHg) or hypercapnia (end-tidal CO(2) = 45 mmHg), which were achieved through adjusting the tidal volume. Systolic arterial pressure (SAP) 15 min after intubation was compared with the preanaesthetic baseline value. Under normocapnia, both TI and P induced a comparable, statistically significant suppression of SAP by approximately 20 mmHg from baseline. Hypercapnia prevented the decrease in SAP in TI but not in P. No patient in the TI-hypercapnia group experienced SAP below 100 mmHg, unlike those in the other groups. In conclusion, mild hypercapnia was effective in the prevention of hypotension in patients receiving thiopental followed by 0.6% end-expiratory isoflurane, but not in patients receiving 6 mg kg(-1) h(-1) propofol.

Topics: Adult; Aged; Aged, 80 and over; Anesthesia, General; Anesthetics, Inhalation; Anesthetics, Intravenous; Blood Pressure; Carbon Dioxide; Female; Heart Rate; Humans; Hypercapnia; Hypotension; Isoflurane; Male; Middle Aged; Monitoring, Intraoperative; Propofol; Respiratory Mechanics; Thiopental

Previous studies in dogs and humans suggest that the carotid body chemoreceptor response to hypoxia is selectively impaired by halothane. The present studies in an open-loop canine preparation were performed to better delineate the effects of anesthetic concentrations of halothane on the carotid body chemoreceptor-mediated phrenic nerve response to an acute hypoxic stimulus.. Three protocols were performed to study the effects of halothane anesthesia on the phrenic nerve response to 1 min of isocapnic hypoxia (partial pressure of oxygen [PaO2] at peak hypoxia, 35-38 mmHg) in unpremedicated, anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. In protocol 1, the dose-dependent effects of halothane from 0.5-2.0 minimum alveolar concentration (MAC) on the hypoxic response during moderate hypercapnia (partial pressure of carbon dioxide [PaCO2], 60-65 mmHg) were studied in 10 animals. In protocol 2, the hypoxic responses at 1 MAC halothane near normocapnia (PaCO2, 40-45 mmHg) and during moderate hypercapnia were compared in an additional four animals. In protocol 3, the hypoxic response of 4 of 10 dogs from protocol 1 was also studied under sodium thiopental (STP) anesthesia after they completed protocol 1.. Protocol 1: Peak phrenic nerve activity (PPA) increased significantly during the hypoxic runs compared with the isocapnic hyperoxic controls at all halothane doses. The phrenic nerve response to the hypoxic stimulus was present even at the 2 MAC dose. Protocol 2: The net hypoxic responses for the two carbon dioxide background levels at 1 MAC were not significantly different. Protocol 3: The net hypoxic response of PPA for the STP anesthetic was not significantly different from the 1 MAC halothane dose. Bilateral carotid sinus denervation abolished the PPA response to hypoxia.. The phrenic nerve response to an acute, moderately severe isocapnic hypoxic stimulus is dose-dependently depressed but not abolished by surgical doses of halothane. This analysis does not suggest a selective depression of the carotid body chemoreceptor response by halothane. The observed hypoxic phrenic response was mediated by the carotid body chemoreceptors in vagotomized dogs because bilateral carotid sinus denervation abolished all increases in PPA.

Topics: Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Carbon Dioxide; Carotid Body; Dogs; Dose-Response Relationship, Drug; Halothane; Hypercapnia; Hypoxia; Phrenic Nerve; Respiration; Thiopental; Vagotomy

The purpose of this study was to determine the cumulative effects of brief intervals of hypoxia and hypercapnia on the pulsatile characteristics of the pulmonary arterial circulation of 48-h-old compared with 2-wk-old open-chest Yorkshire pigs while using two different anesthetic regimens: 1) azaperone and ketamine (4 and 12 mg/kg im, respectively) and 2) thiopental sodium (25 mg/kg i.v.). Animals 48 h old were randomly allocated to undergo mild hypoxia (inspired O2 fraction = 0.15), severe hypoxia (inspired O2 fraction = 0.05), or hypercapnia (inspired CO2 fraction = 0.20), whereas animals 2 wk old underwent severe hypoxia or hypercapnia. With use of Fourier analysis, characteristic impedance (Zo), mean input impedance (Zm), impedance moduli, and phase angles were determined. In 48-h-old pigs anesthetized with azaperone-ketamine, neither mild nor severe hypoxia altered Zo, Zm, or pulmonary vascular resistance (PVR), whereas hypercapnia increased Zo by 22% (P < 0.001), which persisted despite a return to normocapnia. In 48-h-old animals anesthetized with thiopental, baseline control Zo and Zm were lower than those in same-age pigs anesthetized with azaperone-ketamine. In thiopental-anesthetized 48-h-old pigs, both severe hypoxia and hypercapnia increased Zm and PVR but Zo was unaltered. In 2-wk-old pigs anesthetized with thiopental, severe hypoxia but not hypercapnia elevated Zm and PVR, whereas Zo was not changed with either stress. Results indicate age- and anesthetic-dependent responses of Zo, Zm, and PVR to severe hypoxia and hypercapnia. The persistent elevation in Zo caused by hypercapnia indicates a prolonged decrease in arterial compliance or a reduction in effective proximal pulmonary arterial radius.

Topics: Airway Resistance; Animals; Animals, Newborn; Azaperone; Blood Gas Analysis; Energy Metabolism; Female; Hemodynamics; Hypercapnia; Hypoxia; Ketamine; Lung; Male; Pulmonary Alveoli; Pulmonary Circulation; Swine; Thiopental; Transducers, Pressure; Vascular Resistance

The influence of arterial O2 and CO2 tensions on electroconvulsive seizure duration was investigated in five mongrel dogs under consistent anaesthetic conditions. Seizure durations were measured in a randomized protocol of nine possible combinations of arterial gas tension spanning increased, normal or decreased levels of PaO2 and PaCO2. Seizure duration was directly related to PaO2 (p less than 0.00001) and inversely related to PaCO2 (p less than 0.0001). A significant synergism was evident at the extremes of PaO2 and PaCO2, with seizure duration being greater than predicted for hyperoxia-hypocapnia and hypoxia-hypercapnia and shorter than predicted for hypoxia-hypocapnia and hyperoxia-hypercapnia. We conclude that arterial gas tensions strongly influence ECT-induced seizure duration and through this may influence the therapeutic efficacy of electroconvulsive therapy.

Topics: Animals; Blood Gas Monitoring, Transcutaneous; Dogs; Electroconvulsive Therapy; Hypercapnia; Hypoxia; Male; Respiration, Artificial; Seizures; Thiopental; Time Factors

Mean hemispheric cerebral blood flow (CBF) was studied in 11 comatose brain-injured patients following intravenous administration of xenon-133. Repeated measurements were performed in order to evaluate cerebral vasoreactivity following a decrease in PaCO2. In addition, the effect of induced barbiturate coma was evaluated in patients with intracranial hypertension. The cerebral vasoreactivity and the CBF response following induction of barbiturate coma varied. In patients with normal CO2 reactivity, barbiturate treatment was accompanied by a considerable decrease in CBF as compared to patients with decreased or abolished CO2 response. During barbiturate treatment the intracranial pressure (ICP) became normal in three of four patients with preserved CO2 response, but reached normal levels in only one of five patients with impaired CO2 reactivity. Patients whose ICP became normal recovered. The data suggest a positive correlation between CO2 reactivity and the effect of barbiturate treatment. Furthermore, preserved cerebral vasoreactivity after severe head injury may be of prognostic value.

Topics: Adolescent; Adult; Aged; Blood Pressure; Brain Injuries; Carbon Dioxide; Cerebrovascular Circulation; Female; Humans; Hypercapnia; Intracranial Pressure; Male; Middle Aged; Thiopental

The hemodynamic effects of changes in PaCO2 during intermittent positive pressure ventilation (IPPV) were studied in nine dogs with acute cardiac tamponade. During steady state light thiopental anesthesia, measurements were performed during hypocarbia (24.0 +/- 2.6), normocarbia (40.4 +/- 2.4), and hypercarbia (56.8 +/- 3.1 mm Hg; mean +/- SD). The study was carried out at a standardized level of cardiac tamponade that gave a 60% reduction in cardiac output (CO) at normocarbia. Changes in airway pressure were avoided by adding CO2 to the inspiratory gas to obtain the desired PaCO2. Hypercarbia increased pericardial pressure 2-4 mm Hg and significantly decreased CO. During hypocarbia CO increased as pericardial pressure decreased 3-6 mm Hg. These findings are the reverse of changes seen when tamponade is not present. The changes in pericardial pressure most likely influence myocardial tone and cardiac volume and, thus, CO. The results suggest that patients with cardiac tamponade requiring general anesthesia should not breathe spontaneously if there is any danger of respiratory depression and hypercarbia.

Topics: Acute Disease; Anesthesia, Intravenous; Animals; Carbon Dioxide; Cardiac Tamponade; Dogs; Hemodynamics; Hypercapnia; Intermittent Positive-Pressure Ventilation; Positive-Pressure Respiration; Thiopental

To study the significance of normalization of ventilatory or thermal homeostasis during naloxone reversal, 95 patients were given naloxone after thiopental-N2O-O2-relaxant anaesthesia supplemented with fentanyl (6 microgram/kg/h). If naloxone 0.16 mg was given to combat postoperative apnoea during hypercapnia (end tidal carbon dioxide concentration (ETco2)8%), minute ventilation and respiratory rate were significantly higher during the first minutes as compared to the normocapnic patients. Shivering occurred in 44% in the hypercapnic group, as compared to about 30% if naloxone was given during normocapnia (ETco2 5%). Postoperative pain and restlessness were significantly increased in the hypercapnic group. During normocapnia, untoward reactions were less frequent (40%) if naloxone was given in smaller increments (0.08 + 0.08 mg) rather than in one dose (0.16 mg) (72%). This was mainly due to nausea (8% compared to 32%). The incidence and severity of shivering showed a positive correlation to the duration of anaesthesia (r = 0.42) and to the total amount of fentanyl (r = 0.32), but not to the actual postoperative oesophageal temperature (r = -0.13). The results indicate that though untoward reactions after naloxone reversal are aggravated by naloxone-induced normalization of deranged homeostatic mechanisms, their aetiology probably should be sought in an acute abstinence syndrome.

Topics: Adult; Aged; Akathisia, Drug-Induced; Anesthesia, General; Body Temperature; Female; Fentanyl; Homeostasis; Humans; Hypercapnia; Male; Middle Aged; Naloxone; Nitrous Oxide; Respiration; Shivering; Thiopental

Topics: Alfaxalone Alfadolone Mixture; Anesthesia, General; Animals; Cats; Humans; Hydroxybutyrates; Hypercapnia; Neuroleptanalgesia; Plethysmography; Respiration; Thiopental; Tidal Volume; Time Factors

We have assessed the impact of thiopentone on the hypoxic ventilatory reflex, and on the responses to carbon dioxide and doxapram. Thiopentone sedation did not detectably alter any of these aspects of ventilatory control. Thiopentone anaesthesia reduced ventilation and the ventilatory responses to hypoxia, carbon dioxide and doxapram, all approximately in paralle. We conclude that, in contrast to halothane, thiopentone does not selectively reduce the ventilatory response to hypoxia. During light thiopentone anaesthesia, a reasonably brisk hypoxic response is present.

Topics: Adolescent; Adult; Anesthesia; Female; Humans; Hypercapnia; Hypnotics and Sedatives; Hypoxia; Male; Respiration; Thiopental

A case of cardiac arrest is presented which was caused by improper connection of a modified Mapleson D circuit (Bain breathing circuit). Excessive enternal deadspace was created by interchanging the gas inflow line and the attachment for an airway pressure manometer. This resulted in a marked respiratory acidosis, clinically undetected until the concomitant hypoxia produced a severe cardiac depression and arrest. The sequence of events was reproduced in a dog under comparable anaesthetic conditions. In order to avoid this error it is recommended to permanently fuse the connecting piece placed in the circuit with the tubing leading to the airway pressure manometer of the respirator.

Topics: Adolescent; Anesthesia, Inhalation; Animals; Carbon Dioxide; Dogs; Female; Halothane; Heart Arrest; Humans; Hydrogen-Ion Concentration; Hypercapnia; Male; Nitrous Oxide; Oxygen; Succinylcholine; Thiopental

Forty-seven patients undergoing elective/emergency surgery were investigated for the recovery pattern by numerically scoring the state of consciousness, skeletomuscular tone, respiration and blood pressure after the neuromuscular transmission at the level of thenar muscles returned to normalcy. Anaesthesia in them consisted of thiopentone induction and passive ventilation with nitrous oxide and oxygen mixtures (4 1/2:2 1/2 1) with consequent changes in PaCO-2 (22.0 to 90 mm Hg) after using 0.43 to 0.68 mg/kg d-tubocurarine or 2.3 to 3.8 mg/kg gallamine. In this series twelve patients were selected at random and biological assay of cerebrospinal fluid in them for curare/gallamine after 15 min anaesthesia and in the recovery phase was carried out on frog rectus muscle. All the patients recovered satisfactorily and did not present clinical signs of depression of central nervous system, even though all of them showed the presence of curare (ranging from 0.05 to 0.33 mug/ml) and gallamine (from 0.1 to 0.75 mug/ml) in the cerebrospinal fluid. This study therefore indicates that thiopentone, nitrous oxide and relaxant type of anaesthesia does not cause clinical syndrome of post-operative paralysis even when mild to moderate degree of hypocapnia is present and even when such a technique of anaesthesia is administered in poor-risk patients with associated changes in acid-base balance, electrolytes etc. Significant quantities of skeleto-muscular relaxant drug (used during the technique) when found in cerebrospinal fluid after the technique of anaesthesia need not induce post-operative paralysis in man.

Topics: Adult; Anesthesia, General; Blood Pressure; Carbon Dioxide; Consciousness; Female; Gallamine Triethiodide; Humans; Hypercapnia; Male; Muscle Relaxants, Central; Muscle Tonus; Neuromuscular Blocking Agents; Nitrous Oxide; Paralysis; Partial Pressure; Respiration; Respiration, Artificial; Thiopental; Tubocurarine

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in seven chronically tracheostomized dogs awake and during anesthesia with pentobarbital (30 mg/kg, iv), ketamine, or thiopental (10 and 15 mg/kg, respectively, followed by infusion). Isocapnic hypoxic ventilatory drive (HVD) was expressed as the parameter A such that the higher the A, the greater the hypoxic drive. HVD(A) was significantly reduced from 259 +/- 28 (mean +/- SEM) in awake dogs, to 96 +/- 14 after pentobarbital, 161 +/- 27 after thiopental, and 213 +/- 23 after ketamine. Hypercapnic ventilatory drive (HCVD) as measured by S (slope of the VE-PACO2 response curve) was significantly reduced from 1.3 +/- .32 in awake dogs to 0.4 +/- .13 after pentobarbital, 0.5 +/- .12 after thiopental, and 0.6 +/- .11 after ketamine. In addition, hypercapnia-induced augmentation of hypoxic drive was markedly diminished by the two barbiturates but was unaffected by ketamine. Therefore, ketamine at this dose level afforded greater protection during exposure to hypoxia than did barbiturates. (Key words: Ventilation, hypoxic response; Hypoxia, ventilation; Oxygen, ventilatory response; Carbon dioxide, ventilatory response; Anesthetics, intravenous, ketamine; Anesthetics, intravenous, thiopental; Hypnotics, barbiturates, pentobarbital.)

Topics: Anesthesia, Intravenous; Animals; Carbon Dioxide; Dogs; Female; Hypercapnia; Hypoxia; Ketamine; Male; Oxygen Consumption; Pentobarbital; Respiration; Thiopental

Topics: Anesthesia, General; Atropine; Blood Gas Analysis; Blood Pressure; Capillary Resistance; Heart Rate; Humans; Hydrogen-Ion Concentration; Hypercapnia; Methoxyflurane; Nitrous Oxide; Outpatient Clinics, Hospital; Oxygen; Preanesthetic Medication; Surgery, Oral; Thiopental

Topics: Acidosis; Adolescent; Alkaline Phosphatase; Anesthesia, Inhalation; Anesthetics; Appendectomy; Aspartate Aminotransferases; Basal Metabolism; Clinical Enzyme Tests; Creatine Kinase; Fever; Halothane; Hernia, Inguinal; Humans; Hypercapnia; L-Lactate Dehydrogenase; Liver; Male; Muscular Diseases; Nitrous Oxide; Pneumothorax; Succinylcholine; Thiopental

Topics: Adult; Blood Flow Velocity; Blood Pressure; Carbon Dioxide; Cardiovascular System; Curare; Cyclopropanes; Halothane; Heart Rate; Humans; Hypercapnia; Hyperventilation; Narcotics; Respiration; Respiratory Function Tests; Tachycardia; Thiopental; Vascular Resistance

Topics: Animals; Arrhythmias, Cardiac; Dogs; Drug Synergism; Epinephrine; Halothane; Heart; Hypercapnia; Hyperventilation; Rabbits; Thiopental

Topics: Analysis of Variance; Anesthesia, General; Apnea; Arrhythmias, Cardiac; Blood Specimen Collection; Bronchoscopy; Carbon Dioxide; Catheterization; Cyanosis; Female; Humans; Hypercapnia; Hyperventilation; Lidocaine; Male; Middle Aged; Oxygen; Oxygen Consumption; Positive-Pressure Respiration; Succinylcholine; Thiopental; Vocal Cords

Topics: Anesthesia, General; Anesthetics; Animals; Chloroform; Dogs; Ethyl Ethers; Halothane; Hypercapnia; Hypoxia; Methoxyflurane; Statistics as Topic; Thiopental; Trichloroethylene

Topics: Acidosis; Blood Gas Analysis; Carbon Dioxide; Cardiac Surgical Procedures; Heart; Heart Septal Defects; Heart Septal Defects, Atrial; Heart, Artificial; Hypercapnia; Hypothermia; Hypothermia, Induced; Metabolism; Preanesthetic Medication; Succinylcholine; Thiopental; Thoracic Surgery

Topics: Animals; Barbiturates; Brain; Carbon Dioxide; Cerebrovascular Circulation; Dogs; Electrophysiological Phenomena; Electrophysiology; Hexobarbital; Hypercapnia; Hypoxia, Brain; Pentobarbital; Pharmacology; Research; Thiopental