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The Doppler ultrasound (DUS) technique is a widely accepted non-invasive technique to estimate systolic blood pressure (SBP) accurately in paediatric patients. The DUS has a number of limitations. A new pulse monitor, Mr Pulse (MP), operating on the principle of a finger plethysmograph, was developed to offer an alternative technique to estimate SBP. From 104 paired SBP measurements taken in 16 paediatric patients undergoing general anaesthesia, SBP determined by the MP technique correlated closely with that by the standard DUS technique (r2 = 0.98). Analysis of degree of agreement performed indicated that there was good agreement between SBP obtained by the MP and the DUS techniques. The mean +/- standard deviation of differences in paired SBP values between the two measurement techniques was 0.55 +/- 3.59 mmHg. Mr Pulse is as accurate as the DUS technique in estimating SBP and has the advantage of less critical sensor positioning as it is not subject to electrical interference. It has no electrical hazard.

Current methods of forcing end-tidal PCO2 (PETCO2) and PO2 (PETO2) rely on breath-by-breath adjustment of inspired gas concentrations using feedback loop algorithms. Such servo-control mechanisms are complex because they have to anticipate and compensate for the respiratory response to a given inspiratory gas concentration on a breath-by-breath basis. In this paper, we introduce a low gas flow method to prospectively target and control PETCO2 and PETO2 independent of each other and of minute ventilation in spontaneously breathing humans. We used the method to change PETCO2 from control (40 mmHg for PETCO2 and 100 mmHg for PETO2) to two target PETCO2 values (45 and 50 mmHg) at iso-oxia (100 mmHg), PETO2 to two target values (200 and 300 mmHg) at normocapnia (40 mmHg), and PETCO2 with PETO2 simultaneously to the same targets (45 with 200 mmHg and 50 with 300 mmHg). After each targeted value, PETCO2 and PETO2 were returned to control values. Each state was maintained for 30 s. The average difference between target and measured values for PETCO2 was +/-1 mmHg, and for PETO2 was +/-4 mmHg. PETCO2 varied by +/-1 mmHg and PETO2 by +/-5.6 mmHg (s.d.) over the 30 s stages. This degree of control was obtained despite considerable variability in minute ventilation between subjects (+/-7.6 l min(-1)). We conclude that targeted end-tidal gas concentrations can be attained in spontaneously breathing subjects using this prospective, feed-forward, low gas flow system.

We determine whether maintaining normocapnia during hyperoxic treatment of carbon monoxide-exposed research subjects improves cerebral oxygen delivery.This experiment used a randomized, single-blinded, crossover design. We exposed 14 human research subjects to carbon monoxide until their carboxyhemoglobin levels reached 10% to 12%. We then treated each research subject with 60 minutes of hyperoxia with or without normocapnia. Research subjects returned after at least 24 hours, were reexposed to carbon monoxide, and were given the alternate treatment. Relative changes in cerebral oxygen delivery were calculated as the product of blood oxygen content and middle cerebral artery velocity (an index of cerebral blood flow) as measured by transcranial Doppler ultrasonography.Maintaining normocapnia during hyperoxic treatment resulted in significantly higher cerebral oxygen delivery compared with standard oxygen treatment (P.05; 95% confidence interval at 60 minutes 2.8% to 16.7%) as a result of the prevention of hypocapnia-induced cerebral vasoconstriction and more rapid elimination of carbon monoxide due to increased minute ventilation.If severely poisoned patients respond like our research subjects, maintaining normocapnia during initial hyperoxic treatment of carbon monoxide poisoning may lead to increased oxygen delivery to the brain. Determining the effect of such a change in conventional treatment on outcome requires clinical studies.

Cerebrovascular reactivity can be quantified by correlating blood oxygen level dependent (BOLD) signal intensity with changes in end-tidal partial pressure of carbon dioxide (PCO2). Four 3-min cycles of high and low PCO2 were induced in three subjects, each cycle containing a steady PCO2 level lasting at least 60 sec. The BOLD signal closely followed the end-tidal PCO2. The mean MRI signal intensity difference between high and low PCO2 (i.e., cerebrovascular reactivity) was 4.0 ± 3.4% for gray matter and 0.0 ± 2.0% for white matter. This is the first demonstration of the application of a controlled reproducible physiologic stimulus, i.e., alternating steady state levels of PCO2, to the quantification of cerebrovascular reactivity. Magn Reson Med 45:1011–1013, 2001. © 2001 Wiley-Liss, Inc.

The currently recommended prehospital treatment for carbon monoxide (CO) poisoning is administration of 100% O(2). We have shown in dogs that normocapnic hyperpnea with O(2) further accelerates CO elimination. The purpose of this study was to examine the relation between minute ventilation (V E) and the rate of elimination of CO in humans. Seven healthy male volunteers were exposed to CO (400 to 1,000 ppm) in air until their carboxyhemoglobin (COHb) levels reached 10 to 12%. They then breathed either 100% O(2) at resting V E (4.3 to 9.0 L min) for 60 min or O(2) containing 4.5 to 4.8% CO(2) (to maintain normocapnia) at two to six times resting V E for 90 min. The half-time of the decrease in COHb fell from 78 +/- 24 min (mean +/- SD) during resting V E with 100% O(2) to 31 +/- 6 min (p0. 001) during normocapnic hyperpnea with O(2). The relation between V E and the half-time of COHb reduction approximated a rectangular hyperbola. Because both the method and circuit are simple, this approach may enhance the first-aid treatment of CO poisoning.

To determine whether end-tidal PCO2 (PETCO2) measurements obtained with two infrared capnometers accurately approximates the arterial PCO2 (PaCO2) in critically ill neonates, simultaneous measurements of PETCO2 were obtained from the distal and proximal ends of the tracheal tube with a sidestream capnometer (Puritan Bennett/Datex--BP/D) and from the proximal end with a mainstream capnometer (Hewlett-Packard-HP) in 20 intubated neonates. Distal sidestream PETCO2 and mainstream PETCO2 correlated with the PaCO2 (r2 = 0.66 and 0.61, respectively) within the range of 26-57 mmHg PaCO2. However, proximal PETCO2 with the sidestream capnometer correlated very poorly (r2 = 0.09) with PaCO2. The slope of the least square regression line for the distal sidestream capnometer, 0.67, was significantly less than that for the mainstream capnometer, 0.78 but both were significantly greater than that for the proximal sidestream capnometer, 0.39 (P less than 0.05). The slope of the regression for the proximal sidestream capnometer did not differ significantly from horizontal. Insertion of the mainstream sensor for the HP capnometer significantly increased the transcutaneous CO2 when compared with preinsertion values. We conclude that both distal sidestream and mainstream capnometry provide accurate estimates of the PaCO2 in critically ill neonates.

We have previously demonstrated that diaphragmatic muscle fatigue can be diagnosed in infants from spectral frequency analysis of the surface diaphragmatic electromyogram. This requires a digital computer, but the analysis takes several days. Spectral frequency changes, however, can be accurately reflected by band pass filtering and expressing the ratio of high-frequency power to low-frequency power. A fall in this ratio of greater than 20% indicates muscle fatigue. Using a simple analog device to obtain this ratio permits the results to be immediately available; we have used this method to study weaning from mechanical ventilators in ten infants. With a successful weaning step there is no significant change in the ratio, whereas an unsuccessful weaning step invariably leads to a decrease in the ratio of greater than 20%, which precedes CO2 retention and clinical deterioration. These data indicate that diaphragmatic muscle fatigue plays an important role in the infant's response to lung disease. Monitoring of the high/low frequency ratio may be helpful in weaning infants from assisted ventilation.

A device using modification of a Pitot tube has been designed for measurement of tidal volume in infants and small children. Its accuracy was compared both n vitro and n vivo to that of a calibrated pneumotachograph (Fleish #1) designed for a similar flow range. In vitro measurement of air flow with the modified Pitot tube (MPT) was within 5% of the pneumotachograph readings over a range of 1-60 l/min. Similar accuracy was found with measurement of tidal volumes from 20 ml to 1 l, delivered by a calibrated volume-cycled ventilator using a variety of inspiratory flow rates. Tidal volume measurements with the MPT were compared to the pneumotachograph using helium, oxygen, carbon dioxide, and a range of nitrous oxide/oxygen mixtures. A manual control was incorporated into the MPT electronics to allow direct measurements of tidal volume with different nitrous oxide/oxygen concentrations. In vivo, the insertion of the MPT into the patient circuit caused no apparent changes in ventilatory parameters in children under 20 kg. Measurement of tidal volumes with the MPT agreed to within 8% of pneumotachograph readings. The low dead space (1.5 cc) and light weight (12 gm) of the MPT confer advantages over the pneumotachograph (15 ml dead space and a weight of 90 gm) for routine use in pediatric anesthesia.

To assess the augmented delta quotient (ADQ) monitor as a monitor of cerebral function during cardiac surgery, we monitored during operation the electroencephalograms of 48 young subjects (aged 2 weeks to 19 yr). We found ADQ patterns produced by cardiopulmonary bypass, hypothermia and general anaesthetic agents correlated with those obtained from a compressed spectral array (CSA) monitor and could be differentiated from changes caused by cerebral ischaemia, except in the youngest group of patients (less than or equal to 18 months) undergoing deep hypothermia (19.4 (SD 0.8) degrees C nasopharyngeal). In all other age groups the ADQ proved to be a simple monitor of the adequacy of cerebral perfusion. Neurological deficit occurred only if the ADQ was abnormal during hypotension for a period exceeding 7 min. ADQ evaluation of cerebral function was limited by events which produced artificially normal ADQ readings such as low amplitude EEG activity and the described isoflurane effect that was demonstrated to occur in some cardiac patients. The results obtained by the ADQ were comparable to those obtained by compressed spectral array and the ADQ was easier to use and interpret.

IN CHILDREN, the compliance of the lung is related to height and vital capacity 1,2,a as is the total compliance of the thorax. 4 If the volume history of the lung is standardized before measurement of compliance early in anaesthesia, there is evidence from adult subjects that values for static compliance differ little from those reported in normal conscious subjects. 5 It has been shown that in normal anaesthetized children, the compliance of the total thorax, lung, and chest wall are related to height and predicted vital capacity and furthermore, that lung compliance measured early in anaesthesia has a value similar to that reported for conscious children. 6,7 This relationship allows compliance to be compared under anaesthesia in normal children and young children with cardiorespiratory disease who are difficult to study in the conscious state. The anaesthetic technique involves the use of halothane, which has no effect upon lung compliance s and d-tubocurarine, which has on occasion caused broncho-constriction ~ which may be associated with a decrease in the lung compliance, a~ In dogs, d-tubocurarine has been found both to reduce lung compliance and to decrease collateral ventilation, n In man, although this relaxant does not produce significant changes in the compliance of the total thorax 12,13 the effects on the lung have not been differentiated from those on the chest wall. An effect upon the lung could be opposed by the effect of muscle relaxation upon the chest wall and abdomen. Since any effect of curare upon the elastic recoil of the lung must influence the results of comparative studies in young children, the static elastic recoil of the total thorax, lung, and chest wall was measured before and after the intravenous administration of this agent to 10 normal children. METHODS The subjects studied were 10 children aged 7-15 years, with no evidence of cardio-pulmonary disease, who were undergoing orthopaedic operations. Anaesthesia was induced with thiopentone, 5 mg/kg, with atropine, 0.02 rag/ kg. A cuffed endotracheal tube was passed under succinylcholine paralysis and an oesophageal balloon inserted to the lower oesophagus. When spontaneous

Because anaesthesia and artificial ventilation may be associated with reduction of FRC leading to hypoxaemia, we measured changes in FRC and compliance during anaesthesia (0.5 per cent to 1 per cent methoxyflurane) and artificial ventilation in children with normal respiratory function undergoing operation on the limbs and in children with congenital cardiac anomalies undergoing surgical correction. After induction of anaesthesia in the normal children FRC fell in 35 per cent and remained at a fairly steady level throughout the operation. The lesser post-induction fall of 20 per cent observed in the children undergoing cardiac surgery was followed by a continued decrease in FRC during the surgical operation. At the end of operation the reduction in FRC was of similar magnitude in each group of children.

This paper is the first part of a report on a method of measuring FRC by the helium dilution method in anaesthetized children during artificial ventilation. It describes laboratory investigations of the effects of different concentrations of oxygen, nitrogen and methoxyflurane upon the accuracy with which known volumes can be determined in a “dummy lung.” For a volume of 500 ml the coefficient of variation was

It is generally believed that there is a scarcity of muscle spindles in the diaphragm and that there is no tonic activity at end expiration. This conclusion is based mainly on animal studies and the difficulty in differentiating tonic electromyogram activity from noise. We have, however, found a number of muscle spindles in the newborn human diagphragm, concentrated in the region of the central tendon. We also tried to detect tonic activity by decreasing it (by rapid-eye movement (REM) sleep or anesthesia) or increasing it (with abdominal loading). During REM sleep in five infants and five adults, using subcostal electrodes were observed a marked fall in tonic activity (P less than 0.001) compared to non-REM or quiet sleep. We also observed a reduction in diaphragmatic tonic activity with halothane anesthesia (P less than 0.001). With esophageal electrodes in adult subjects, there was a rise in tonic diaphragmatic activity proportional to the amount of abdomina load (P less than 0.001). We conclude that there are muscle spindles in the human diaphragm and that there is tonic activity at end expiration.