Yoshio Ohta

Pressure support ventilation augments spontaneous breathing with improved thoracoabdominal synchrony in neonates with congenital heart disease

In neonates, during spontaneous breathing with demand-type continuous positive airway pressure (CPAP), high airway resistance caused by small endotracheal tubes, time delay for triggering, and rapid respiratory frequency may result in patient-ventilator asynchrony. Such asynchrony may alter normal breathing patterns and thoracoabdominal synchrony. We, therefore, studied whether pressure support ventilation (PSV) could augment spontaneous breathing and improve synchrony between the rib cage (RC) and the abdominal (AB) motions in nine postoperative neonates with congenital heart disease. Three successive levels of PSV (0, 5, and 10 cm H2 O) were used randomly. With increasing levels of PSV, the tidal volume (VT) increased and the respiratory frequency decreased, associated with an increase in minute ventilation. To assess thoracoabdominal synchrony, maximum compartment amplitude (MCA)/VT (MCA = AB + RC) and the phase delay of the RC-to-AB motion during inspiration (the ratio of the time delay to the inspiratory time) were measured using respiratory inductive plethysmography. When the motions of the RC and AB were out of phase, MCA/VT exceeded 1.0. MCA/VT decreased significantly from 1.3 +/- 0.3 without PSV to 1.0 +/- 0.0 with PSV of 10 cm H2 O. The phase delay and paradoxical motion of the RC observed in seven of the nine cases without PSV also disappeared with PSV of 10 cm H2 O. In conclusion, PSV can effectively augment spontaneous breathing with better thoracoabdominal synchrony in neonates. Implications: Assisting spontaneous ventilation in a neonate is often difficult. Because pressure support ventilation facilitates coordination between the patient and ventilator in adults and children, we thought it might be effective in neonates. Our study supports this conclusion. (Anesth Analg 1997;85:789-93)

Inspiratory pressure-volume curves at different positive end-expiratory pressure levels in patients with ALI/ARDS.

Background: In lung protective strategy, positive end‐expiratory pressure (PEEP) slightly higher than the Pflex (the airway pressure corresponding to the lower inflection point (LIP) on the inspiratory pressure–volume (P‐V) curve measured with ZEEP) is generally recommended. However, this method to determine optimal PEEP lacks a theoretical background and there is no clinical report that investigated how the P‐V relationship would be with such PEEP. Therefore, we measured inspiratory P‐V curves at different PEEP levels to increase our knowledge about the inspiratory P‐V curve with PEEP.

Transient renal tubular dysfunction in a patient with severe asthmatic attack treated with sevoflurane.

of 9 h on the first and second hospital days. However, because isoflurane could not reduce the irritability of his airway, the control of ventilation was difficult with isoflurane. We therefore replaced the drug with sevoflurane. Inhalation anesthetics were passed from a vaporizer and added to a humidifier system attached to a ventilator (Puritan-Bennett 7200ae). Soda lime was not used. Inhaled isoflurane and sevoflurane concentration varied between 0.25% and 6.0% to provide bronchodilation. The end-tidal concentrations of the inhalation anesthetics were continuously measured with an anesthetic analyzer (Capnomac, DATEX, Helsinki). The minimum alveolar concentration (MAC) hours of administered sevoflurane was 298 MAC hours. The agecorrected MAC of sevoflurane in this case was 1.3%. Figure 1 shows the serum and urinary inorganic fluoride concentrations during and after the administration of sevoflurane. The serum inorganic fluoride concentration increased to over 50 μmol·l21, and its maximum level was 70.5 μmol·l21. The maximum urinary inorganic fluoride concentration was 2047 μmol·l21. During sevoflurane administration, the urinary inorganic fluoride concentration did not decrease. Figure 2 plots the urinary concentrations of N-acetyl-â-d-glucosaminidase (NAG) and â-2-microglobulin (BMG). The urinary NAG and BMG concentrations were abnormally elevated, and their maximum levels were 52.3U·l21 and 86 000μg·l21. These concentrations decreased gradually from the 15th day. The serum BMG concentration was in the normal range (data not shown). Figure 3 shows the data on the urinary volume and daily urinary excretion of NAG and BMG. The daily excretion of NAG and BMG was abnormally elevated, reaching a maximum of 137.5 U·day21 and 238.7mg·day21, respectively. The volume of urine was large (2–6 l daily), but its specific gravity was in the normal range. The values of blood urea netroge (BUN), serum creatinine, and creatinine clearance were normal. In the phenolsulfonphthalein (PSP) excretion test, the value at 15min

Interaction Between Muscle Relaxants

In Japan, two groups of muscle relaxants are commonly used clinically. One of them is depolarizing relaxant; succinylcholine and the other is nondepolarizing aminosteroidal relaxants; vecuronium and pancuronium. Considering that depolarizing relaxants are basically agonist and nondepolarizing relaxants are antagonist to the nicotinic acetylcholine receptors on the motor endplate, it is not unexpected that their neuromuscular effects are mutually inhibitory. Accordingly, pretreatment with a subparalyzing dose of nondepolarizing relaxant antagonizes subsequent succinylcholine-induced neuromuscular block. However, when the sequence of administration is reversed and an intubating dose of succinylcholine was followed by a nondepolarizing relaxant, potentiation rather than antagonism of the latter block has been reported. In my presentation, this controversial interaction between succinylcholine and subsequently administered aminosteroids will be discussed.

Halothane augments the interaction between succinylcholine and pancuronium.

We previously reported that prior administration of succinylcholine prolonged the pancuronium-induced neuronmuscular block during halothane anesthesia [1]. Recent publications [2-3], however, have reported conflicting results in which the same dose of succinylcholine did not affect the duration of the pancuronium-induced neuromuscular block during neuroleptanesthesia. Therefore, it is possible that halothane may have affected our previous results. The present study was performed to investigate if halothane augments the interaction between succinylcholine and pancuronium. The Study was approved by the local Ethics Committee. Informed consent was obtained from 30 adult patients (ASA class I; aged 18-60 years), none of whom was taking medication or suffering from an illness known to affect neuromuscular function. All patients were premedicated with a combination of pethidine 1 mg.kg 1 and atropine 0.01 mg.kg <, i.m. 1 h before induction of anesthesia. They were randomly divided into groups of the same size according to the anesthetic agents used. The two groups were similar in age and weight. In the neuroleptanesthesia (NLA) group (n = 15), anesthesia was induced with droperidol 0.15 mg.kg -1, thiopental 2mg.kg -1, and fentanyl 45 ~g.kg -1, and the trachea was intubated with a cuffed tube facilitated by transtracheal administration of 4% lidocaine. Anesthesia was maintained with 60% nitrous oxide in oxygen with intermittent administration of thiopental and fentanyl. In the halothane group

Effect of Isoflurane and Sevoflurane on the Potencies of the Neuromuscular Blocking Agents in Rat in Vivo

It has been reported that Isoflurane1 and Sevoflurane2 increases the neuromuscular (NM) blocking potencies of the muscle relaxants (MR). In this study the effect of these two inhalation anesthetics at 1.25 MAC and 2.25 MAC on the potencies of vecuronium, rocuronium and the new steroidal agent SZ1676 were studied.