Kazuo Fukumitsu

Duration of Apnea in Anesthetized Infants and Children Required for Desaturation of Hemoglobin to 95%The Influence of Upper Respiratory Infection

Sixty-one patients ASA physical status 1-2 aged 1 month to 12 years undergoing elective surgery were included in the study. Anesthesia was induced via a mask with sevoflurane up to 5% and 66% nitrous oxide in oxygen. After paralysis with vecuronium (0.12 mg/kg iv), the trachea was intubated and the lungs were ventilated manually with 3% sevoflurane in oxygen until the end-tidal nitrous oxide decreased to less than 5%. Apnea was started by disconnecting the breathing circuit from the endotracheal tube. The time from the start of apnea to Spo2 of 95% was measured. Manual ventilation was reinstituted when Spo2 decreased to 95% and another set of vital signs was recorded. Twenty of 61 patients had symptoms of upper respiratory infection. The time to Spo2 of 95% correlated well with height, age, and body weight both by linear and non-linear regression analyses. The patients with symptomatic upper respiratory infection required less time for Spo2 to decrease to 95% compared to the asymptomatic children. We conclude that younger children require less time for Spo2 to decrease to 95%. The presence of upper respiratory infection is an additional factor increasing the susceptibility of small children to hypoxemia.

Duration of apnoea in anaesthetized children required for desaturation of haemoglobin to 95%: comparison of three different breathing gases.

In this study, we compared three gas compositions to determine if the duration of apnoea for Spo2 to decrease is proportionate to the oxygen fraction of the gas prior to apnoea. Twenty‐five patients ASA physical status 1–2 aged two months to 12 years were included in the study. Anaesthesia was induced via a mask with 5% sevoflurane and 66% N2O in oxygen. After paralysis with vecuronium (0.12 mg·kg−1, i.v.) the trachea was intubated and anaesthesia was maintained with sevoflurane and N2O in oxygen. When cardiovascular stability was obtained, the patient was randomly set to breathe one of three gas compositions: 1. oxygen (Fio2 1.0), 2. N2O/O2 (Fio2 0.4), and 3. air/O2 (Fio2 0.4). All three gas compositions included 2–4% of sevoflurane to maintain anaesthesia. After more than eight min of each gas breathing, apnoea was begun by disconnecting the breathing circuit from the tracheal tube. The time from the start of apnoea (Spo2 100%) to Spo2 of 95% (T95) was measured. T95 measured after breathing N2O/O2 and air/O2 were 34.6 ± 5.7 and 28.8 ± 4.7% of that measured after oxygen breathing (P < 0.001 vs oxygen breathing, P < 0.001 vs oxygen and N2O/O2 breathing), respectively. Preoxygenation before intubation was validated to delay the haemoglobin desaturation brought about by apnoea. An induction technique using a low Fio2 will allow rapid haemoglobin desaturation.

Comparison of recorded values from six pulse oximeters.

Recorded values (SpO2) of oxygen saturation from six noninvasive pulse oximeters were compared to each other and to the value from a cooximeter. Simultaneous measurements were obtained from each instrument in eight healthy nonsmoking volunteers rendered hypoxic greater than 70% SpO2. Functional arterial oxygen saturation (SaO2), fractional SaO2 (%HbO2), and percent fraction of carboxyhemoglobin (HbCO) and methemoglobin (MetHb) were determined by a cooximeter. The difference between SaO2 and %HbO2 was 2.3 +/- 0.3 (SD) % (p less than .001) with 1.4 +/- 0.1% HbCO and 0.9 +/- 0.1% MetHb. The SpO2 values in two instruments were close to %HbO2, while the other instruments correlated approximately with SaO2. The greatest SpO2 difference among the instruments was 2.7 +/- 1.9% (p less than .001). These results may indicate that, under normal dyshemoglobin levels, some pulse oximeters are calibrated to estimate SaO2 and others to estimate %HbO2. Since the pulse oximeter using two wavelengths cannot measure accurately %HbO2 or SaO2 in the presence of dyshemoglobin, SpO2 values would be independent from %HbO2 and SaO2. A standard calibration method for pulse oximeters should be established by the manufacturers.

A new modification of anaesthesia mask for fibreoptic intubation in children.

We made a paediatric anaesthesia mask suitable for fibreoptic intubation by modifying a commercially available disposable mask with a ventilation port (Vent port) on a side. We added a large fibreoptic port (FO port, 22 mm in ID) in the middle of the mask to allow the passage of all sizes of paediatric tracheal tubes. This FO port was covered with an elastic rubber membrane to allow air‐tight fibrescopic manipulation. Fibreoptic intubation was performed safely through the FO port under continuous manual ventilation with anaesthetic gases via a Vent port connected to the breathing circuit. We succeeded in tracheal intubation in several infants and children with difficult airway in less than ten min, mainly via the nasotracheal route. This fibreoptic mask provides a safer technique for fibreoptic intubation in patients with difficult airways, especially in infants and small children.

A rare case of upper airway obstruction in an infant caused by basal encephalocele complicating facial midline deformity.

A four‐month‐old male infant with basal encephalocele of the transsphenoidal type presented with upper airway obstruction and facial midline deformity, including cleft lip, cleft palate, hypertelorism and exophthalmos. Basal encephalocele is a rare disease, and usually not detectable from the outside. In this case, initially the cause of an upper airway obstruction was considered to be posterior rhinostenosis, and posterior rhinoplasty with inferior nasal conchectomy was scheduled. However, in preoperative examination, computed tomography (CT) and magnetic resonance imaging (MRI) revealed a bony defect in the sphenoidal bone and a cystic mass in communication with cerebrospinal fluid, herniating into the nasal cavity through the bony defect. The mass was diagnosed as a transsphenoidal encephalocele, the scheduled operation cancelled, and tracheostomy performed for airway management. The possibility of basal encephalocele should be considered in the case of upper airway obstruction with facial midline deformity.

ROLES OF BETA 1- AND BETA 2-ADRENOCEPTORS IN THE MECHANISM OF HALOTHANE MYOCARDIAL SENSITIZATION IN DOGS

The authors investigated the comparative roles of beta 1- and beta 2-adrenoceptors in myocardial sensitization by halothane in dogs. The arrhythmogenic dose (AD) of isoproterenol was determined in the presence of various doses of phenylephrine during halothane anesthesia in dogs, and the influences of 1-metoprolol (beta 1-antagonist) and ICI-118,551 (beta 2-antagonist) on the AD were examined. In the presence of 1-metoprolol, the AD of isoproterenol was significantly greater than the control, but in the presence of ICI-118,551, the AD of isoproterenol was lower. Blood pressure during the arrhythmias was higher in the presence of ICI-118,551 than that in controls. In addition, the AD of ritodrine (beta 2-agonist) was also determined at various doses of phenylephrine. The interaction between phenylephrine and ritodrine in inducing arrhythmias showed hyperbolic isoboles. However, 1-metoprolol completely inhibited the occurrence of arrhythmias induced by ritodrine and phenylephrine. The results suggest that myocardial beta 1-adrenoceptors play an essential role in the genesis of arrhythmias during halothane anesthesia in dogs, whereas beta 2-adrenoceptors do not.

Postbypass pulmonary artery pressure influences respiratory system compliance after ventricular septal defect closure

It is reported that surgical correction of left‐to‐right shunt improves respiratory function in paediatric cardiac patients. However, such correction sometimes does not result in an improvement of respiratory compliance. The purpose of this study was to look for factors determining changes in respiratory system compliance (Crs) in patients who underwent closure of ventricular septal defect (VSD closure). In a prospective study, 17 children (< 10 kg) who underwent VSD closure were enrolled. They were divided into two groups, according to postbypass mean pulmonary artery pressure (mPAP). The patients were allocated to Group C if mPAP was ≤ 18 mmHg (n=12) and to Group PH if > 18 mmHg (n=5). We compared the ratio of postoperative Crs to preoperative Crs (Cpost/Cpre) between the groups. A multiple occlusion technique was used to measure Crs. The Cpost/Cpre in group C was larger than that in group PH (1.11 ± 0.17 vs. 0.81 ± 0.12, P < 0.01). There was a correlation between postbypass mPAP and Cpost/Cpre (rs=0.49, P < 0.05), but no correlation was noted between preoperative mPAP, Qp/Qs or Rp/Rs and Cpost/Cpre. We concluded that high postbypass mPAP was associated with a perioperative decrease in Crs after VSD closure.

Brachial plexus birth injuries: anaesthesia for surgical nerve reconstruction and preoperative myelography and computed tomographic myelography.

Surgical nerve reconstruction for brachial plexus birth injuries and preoperative myelography and computed tomographic (CT) myelography require special anaesthetic considerations. Anaesthesia and medical records were retrospectively reviewed for the infants who underwent myelography, CT myelography (n=37) and microsurgical nerve reconstruction (n=34) at our institution from January 1993 to August 1996. Anaesthetic considerations include long duration of operation, perioperative respiratory complications and plaster application which makes reintubation difficult. Myelography for diagnosis requires a specific positioning of the patient with the head fixed in a midline and prone position.

Effects of pentazocine and other opioids on the potassium-evoked release of [3H]noradrenaline from guinea pig cortical slices

Noradrenaline release and its modulation via presynaptic opioid receptors were examined in guinea pig cortical slices. Slices preloaded with [3H]noradrenaline were superfused in the presence of desipramine (1 microM) and were stimulated by 16 mM K+. 1-Pentazocine inhibited the K+-evoked release of [3H]noradrenaline in a dose-dependent manner (3 x 10(-7)-10(-5) M), while d-pentazocine did not inhibit. This inhibitory effect of 1-pentazocine was antagonized by Mr 2266 (10(-6) M) but not by naloxone (10(-6) M). Among other opioids, dynorphin A-(1-13) and ethylketocyclazocine (kappa agonists) decreased the K+-evoked release of [3H]noradrenaline. Tyr-D-Ala-Gly-NMe-Phe-Gly-ol (DAGO, mu agonist) also inhibited [3H]noradrenaline release but was less potent than the kappa agonists. [D-Pen2,D-Pen5]enkephalin (DPDPE, delta agonist) and phencyclidine (sigma agonist) had no effects on the stimulated release of [3H]noradrenaline. Thus, it was shown that kappa receptors are the major subtype of opioid receptor involved in modulation of noradrenaline release in guinea pig cortex, and that 1-pentazocine inhibits the K+-evoked release of noradrenaline through activation of these receptors.

Effect of Local Anaesthetics on the Stimulus-secretion Coupling in Bovine Adrenal Chromaffin Cells*

Abstract— This study was carried out to determine the relative potencies of local anaesthetics to inhibit the cholinergic synaptic transmission using cultured bovine adrenal chromaffin cells, and to clarify if the inhibitory action would correlate with biophysical and pharmacological properties. Local anaesthetics (bupivacaine, etidocaine, tetracaine, lignocaine and procaine; 0·02–2 Mm) inhibited carbachol‐induced catecholamine release from the cells in a concentration‐dependent manner. This inhibition was completely reversible. IC50 (concentration of 50% inhibition) of each anaesthetic showed no correlation with the lipid solubility. The local anaesthetics showed greater inhibitory potency at a higher extracellular pH. The results suggest that clinically relevant concentrations of local anaesthetics inhibit the stimulus‐secretion coupling in the chromaffin cells. The un‐ionized base form plays a major role, and the inhibitory potency does not depend on the lipid solubility of the anaesthetics.