Rapid inhalation induction with halothane-nitrous oxide for myasthenic patients.

Rapid inhalation induction (RII) was successfully employed for patients without myopathy. Inhalatory agents can be used for anaesthetic induction of myasthenics, avoiding the use of neuromuscular blocking agents. We studied the use of RII in 15 myasthenics (MG) and in 15 normal subjects (nMG), measuring induction time (TI), cardiorespiratory effects, complications, and evaluated the patient's reaction to RII. The patients were submitted to elective transsternal thymectomy (MG) and gynaecological or lower abdominal surgery (nMG). No premedication was used. After preoxygenation, RII was started using a mixture of 4% halothane and O2:N2O (1:2). They performed three vital capacity breaths, followed by normal spontaneous ventilation. The TI was assessed by timing the loss of verbal command (TLVC) and loss of eyelid reflex (TLER). Systolic and diastolic pressure, pulse oximetry, capnometry, respiratory rate (RR) and heart rate (HR) were measured during induction at each minute, for four minutes. After a postanaesthetic questionnaire only two normal subjects did not like the RII technique. Mean values for TLVC and TLER were 67 and 73 sec for MG and 64 and 69 sec for nMG, respectively. There was no change in HR for MG or blood pressure. The RR increased in both groups, but no change in PetCO2 was observed; SaO2 was > 97%. In conclusion, RII can be performed rapidly and safely in myasthenic patients and is a technique that should be considered for the induction of anaesthesia in myasthenic patients.

Can anesthesia ventilators provide high-frequency ventilation?

We measured the tidal volumes (VT) delivered by two anesthesia ventilators (the Narkomed 2B and the Ohmeda 7800) to a model lung at frequencies of 60 breaths/min and 99-100 breaths/min under two conditions of compliance and resistance designed to mimic mild and severe adult respiratory distress syndrome (ARDS) (mild ARDS = S1 and severe ARDS = S2). The VT produced were measured with a pneumotachometer at the ventilator outflow and distal to the anesthesia circuit. With the Narkomed 2B, the VT measured at the entrance to the model lung decreased from 216 mL to 129 mL in S1, and from 152 mL to 88 mL in S2 as the ventilatory frequency increased from 60 to 99 breaths/min. With the Ohmeda 7800, the VT decreased from 213 mL to 118 mL in S1, and from 134 mL to 73 mL in S2 when the frequency was changed from 60 to 100 breaths/min. Since the delivered VT are similar to those previously reported to maintain adequate ventilation at these rates using standard high-frequency ventilation (HFV), it may be possible to use these newer anesthesia ventilators for this purpose.

The effect of changing end-expiratory pressure on respiratory system mechanics in open- and closed-chest anesthetized, paralyzed patients.

The decrease in functional residual capacity (FRC) with anesthesia may cause lung volume to decrease below closing volume, thereby impairing oxygenation. Increasing end-expiratory pressure (EEP) reexpands atelectatic areas in anesthetized, ventilated patients, but its effect on pulmonary mechanics is less well understood. We studied the effect of varying EEP on the mechanical behavior of the respiratory system in patients undergoing either closed (Group 1) or open-chest (Group 2) surgical procedures. We measured airway opening pressure (PaO), flow (V), and esophageal pressure (Pes) (in Group 1 only) at EEPs of 0, 2.5, 5, and 10 cm H2O. Dynamic elastance (E) and resistance (R) for the respiratory system (RS), the lung (L), and the chest wall (CW) were estimated by fitting the equation P = RV + EV + K to the measured data by multiple linear regression where P was either Pao, Pes, or Pao-Pes. Group 1 EL decreased with increases in EEP to 5 cm H2O and then began to increase with EEP above this level. The same occurred in Group 2 before opening the chest. After opening the chest in Group 2, EL increased as EEP increased at all values above 0 cm H2O. The magnitudes of RRS and RL were similar in both groups of subjects and in each group these quantities decreased with increases in EEP. Dynamic EL responded differently to changes in EEP in subjects with open-chest and closed-chest procedures. We attribute this difference to overdistension of the remaining ventilable lung tissue at all levels of EEP in open-chest patients.

Post spinal meningitis and asepsis.

BACKGROUND: Post spinal meningitis (PSM) is a complication still currently being reported. After two PSM cases in our hospital an epidemiological study was initiated, which included a survey of techniques for asepsis that are applied in our department. METHODS: Cases defined as PSM comprised meningitis within a week after spinal anesthesia. Anesthesia records, anesthesia complication files and the records of the Hospital Commission for Infection Control from 1997 to 2000 were reviewed. Asepsis techniques applied were surveyed by a questionnaire answered by all our department's anesthesiologists. The equipment and procedures for spinal anesthesia were listed. Current anesthesia textbooks were reviewed for recommendations regarding asepsis techniques in conjunction with spinal anesthesia. RESULTS: Three cases of PSM were identified following 38,128 spinal anesthesias whereas none was observed in 12,822 patients subjected to other types of regional or general anesthesia (P>0.05). Culture of cerebrospinal fluid yielded Streptococcus in two patients and was negative in the other patient. The asepsis technique applied by the anesthesiologists varied considerably. The literature review showed that aspects on asepsis for spinal anesthesia are poorly covered. CONCLUSION: The incidence of meningitis was similar in patients subjected to spinal anesthesia and in those subjected to other anesthetic techniques. Asepsis techniques were found to differ considerably among our staff members, reflecting the lack of well-defined published standards for this procedure. We recommend that asepsis for spinal anesthesia should not be less rigorous than for surgical asepsis.

Respiratory mechanical properties during fentanyl and alfentanil anaesthesia.

The purpose of this study was to assess the effects on respiratory mechanics of fentanyl and alfentanil in 20 subjects to be submitted to coronary artery bypass grafting. Using the end inflation occlusion method (EIOM) we obtained the elastance (E) and resistance (R) of the total respiratory system (rs), thoracic wall (w) and lungs (L). The total respiratory system was divided into thoracic wall and lungs by using an oesophageal catheter. The data were recorded before, immediately after, and two, five and ten minutes after fentanyl and alfentanil iv bolus, at doses of 30 and 120 micrograms.kg-1, respectively. The Ers increased at two, five and ten minutes and the EL at ten minutes after drug administration. The Rrs,min and RL,min increased at two, five and ten minutes and the RL,max at five and ten minutes. Both drugs provoked no change in Ew or Rw. It is concluded that the increased in Rrs,min and RL,min could be explained by opioid bronchoconstriction. No differences were found between the effects of fentanyl and alfentanil on respiratory mechanics.