Pressure testing the anaesthetic machine and breathing system.
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Biomedical subjects
Publications and source records attributed to M P Barrowcliffe.
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In a prospective, double-blind study, we have examined the effect of preoperative nabilone on postoperative nausea and vomiting (PONV). Sixty women, less than 70 yr old, undergoing total abdominal hysterectomy, were allocated randomly to receive either nabilone 2 mg or metoclopramide 10 mg orally 90 min before induction of anaesthesia. The study was designed to detect a 50% difference in the incidence of postoperative vomiting between the two groups, with an 80% power of achieving a statistically significant result at the 5% level. Data from 53 patients were analysed: the incidences of nausea and vomiting for the metoclopramide group were 70% and 67%, respectively; the corresponding values for the nabilone group were 73% and 54%. These differences were not significant.
OBJECTIVE: To assess the role of intravascular atrial electrograms in improving the diagnosis of complex cardiac arrhythmias in critically ill patients. DESIGN: Prospective, clinical study comparing the accuracy of cardiac rhythm diagnosis using standard surface electrocardiogram (EKG) and intravascular atrial electrograms. SETTING: Intensive care unit of a university teaching hospital. PATIENTS: A total of 57 critically ill patients (44 cardiothoracic surgery, five acute myocardial infarction, two septic shock, six miscellaneous) with 85 complex cardiac arrhythmias that were unable to be diagnosed with certainty using the surface EKG. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The intravascular atrial electrogram altered diagnosis based on the surface EKG in 11 (13%) patients and confirmed rhythm diagnosis in 60 (71%) of 85 patients with arrhythmia. Of 61 patients with wide complex tachycardia, 40 (66%) were diagnosed as ventricular tachycardia (atrioventricular dissociation demonstrated on the atrial electrogram), and 11 (18%) as supraventricular tachycardia with aberrant conduction. Ten (16%) wide complex tachycardias could not be diagnosed with confidence using both surface EKG and intravascular electrogram. There were no adverse effects with this technique. CONCLUSIONS: Intravascular atrial electrograms recorded via central venous catheters are useful in the diagnosis of complex cardiac arrhythmias, particularly ventricular tachycardia. The technique is safe, simple, and quick.
To examine how molecular charge affects the transfer of molecules across the alveolar-capillary barrier, we prepared the following dextrans of equivalent molecular size (mol wt 10,000) but varying molecular charge: neutral dextran, cationic DEAE dextran, and anionic dextran sulfate. These were labeled with 99mTc. The lungs of three groups of anesthetized rabbits were insufflated with dextran aerosols, with six rabbits receiving each type, and the half-time pulmonary clearance (t1/2) was measured. Control t1/2's (95% confidence limits) were 95 (74-120), 227 (192-268), and 291 (246-345) min for neutral, cationic, and anionic dextrans, respectively. One week later, when the same animals were restudied 4 h after 3 micrograms/kg iv endotoxin, t1/2's were 102 (75-139), 167 (149-187), and 126 (102-154) min, respectively. After 30 min during this repeat study, animals were ventilated with 20 breaths of cigarette smoke, which acutely increased the clearance rate to 34 (26-46), 25 (20-31), and 13 (7-24) min, respectively. Mean carboxyhemoglobin levels were not significantly different in the three groups: 13.6, 12.7, and 11.1%, respectively. These results demonstrated that neutral dextrans showed the same clearance rate before and after endotoxin, whereas the charged dextrans had a significantly faster clearance after endotoxin. After smoke exposure the anionic dextran left the lung more rapidly than the neutral dextran. Thus molecular charge affects solute transfer across the alveolar-capillary barrier in both normal and injured lungs, and an effect of endotoxin on the lung can be detected with charged dextrans but not with neutral dextran.
The latency of the early cortical wave Nb of the auditory evoked response (AER) was compared with responses to Tunstall's isolated forearm test, while the concentration of nitrous oxide was progressively reduced during light anaesthesia in seven patients. A threshold Nb latency of 44.5 ms was chosen to discriminate between an early cortical AER containing three waves and that with two waves of longer latency. When Nb latency decreased below this threshold, four of the patients has positive responses, indicating awareness. The addition of a volatile anaesthetic abolished any response, and increased Nb latency to more than 44.5 ms. The three wave AER pattern, therefore, is associated with a depth of anaesthesia at which awareness occurs.
In anesthetized rabbits we measured clearance from lung to blood of eight aerosolized technetium-99m-labeled compounds: diethylenetriaminepentaacetate (99mTc-DTPA); cytochrome c; myoglobin; a myoglobin polymer; albumin; and anionic, cationic, and neutral dextrans of equivalent molecular size. We investigated the effect of applying positive end-expiratory pressure (PEEP) and, on a subsequent occasion, of injecting oleic acid intravenously to produce acute lung injury on the pulmonary clearance rate. Base-line clearance rates were monoexponential and varied with the molecular weights of the radiotracers. For each tracer the rate of clearance was increased a similar degree by either PEEP or oleic acid. However, with PEEP, clearance remained monoexponential, whereas after oleic acid, smaller molecular-weight radiotracers had multiexponential clearance curves. This suggests that after oleic acid the alveolar epithelium breaks down in a nonuniform fashion. We conclude that differentiation of the effect of PEEP from that of severe lung injury caused by oleic acid is not readily accomplished by either increasing the size of the tracer molecule or by varying the molecular charge.
We measured pulmonary clearance of aerosolised 99mtechnetium-labelled diethylenetriaminepentacetate (99mTc-DTPA) in thirty-four patients with acute respiratory dysfunction. Results were expressed as a half-time clearance from lung to blood (T1/2). In sixteen non-smoking patients with acute lung injury, clearance was monoexponential, median T1/2 11, range 4-40 min, and in five multi-exponential, median rapid T1/2 3 min, with a slower median T1/2 of 18 min (range 2-4 and 15-31 min respectively). Clearance was significantly (P less than 0.0001) more rapid than normal non-smoking subjects previously studied (median T1/2 70, range 37-182 min). Three smokers with acute lung injury had T1/2S of 5, 18 and 22 min, not significantly (P greater than 0.05) quicker than normal smokers previously studied (median T1/2 20, range 6-73 min). One smoking lung-injured patient had an abnormal multi-exponential 99mTc-DTPA clearance. Four patients with cardiogenic pulmonary oedema had T1/2S within the normal range. Repeated measurements made on nine patients with acute lung injury showed that clearance remained abnormally rapid despite improvements in lung radiographic appearance and gas exchange. We conclude that the 99mTc-DTPA technique provides a virtually non-invasive measure of alveolar-capillary barrier dysfunction in non-smoking patients with acute lung injury.
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The duration of respiratory depression induced by morphine 10 mg/70 kg was studied following the administration of one of two opioid antagonists. Respiratory measurements included: (i) the ventilatory response to carbon dioxide, described in two ways--the minute ventilation at an end-tidal carbon dioxide partial pressure of 8 kPa (VE8) and the log slope of the ventilatory response to carbon dioxide; (ii) resting end-tidal carbon dioxide partial pressure; (iii) rate of ventilation. One hour after administration of morphine, one of the following was given i.v.: nalmefene 0.4 mg/70 kg; naloxone 0.4 mg/70 kg (low dose); naloxone 1.6 mg/70 kg (high dose); or saline placebo. The depression of VE8 by morphine was antagonized by all three treatments for the 1.5 h after the injection. However, for the 1.5-6 h after antagonist, VE8 following naloxone became depressed, whereas VE8 after nalmefene remained significantly increased compared with other treatments. Nalmefene restored the slope of the ventilatory response to baseline for 6 h and differed significantly from low but not high dose naloxone. Resting end-tidal carbon dioxide measurements demonstrated that nalmefene activity exceeded that of low but not high dose naloxone over the 1.5-4.5 h period. Rate of ventilation was not different between treatments.
We examined the effect of intravascular and tissue accumulation of tracer when measuring pulmonary clearance of sodium pertechnetate-labeled diethylenetriamine pentaacetate (99mTc-DTPA). Pigs were intubated with endobronchial tubes, permitting deposition of an aerosol of 99mTc-DTPA only into the left lung. Scintillation detectors recorded radioactivity separately from one thigh and from the lung and chest wall on the left and right side. 99mTc-DTPA was given intravenously after 30 min, so that the chest counts from the left lung could be corrected for background activity in either the right lung or the thigh. The uncorrected clearance half time (t1/2) mean +/- SE from the left chest was 118.5 +/- 14.4 min. When corrected for background activity in the right chest, the t1/2 was 82.1 +/- 10.5 min, and when corrected for background activity in the thigh, the t1/2 was 80.9 +/- 10.6 min. There was no significant difference between t1/2 corrected by the measurements from the right chest or the thigh, and in four of five animals the corrected t1/2 by either method was significantly different from the uncorrected t1/2 (P less than 0.05). There was no correlation between the uncorrected t1/2 and the magnitude of the required correction. We conclude that correction for intravascular and tissue accumulation of tracer is an important refinement of the technique and can easily be accomplished by measuring accumulation of tracer in the thigh.
A method has been developed for producing 'kits' for labelling porphyrins, dextrans, myoglobin and cytochromes with technetium-99m. The kits have a shelf life of at least 3 months and can be reconstituted by the simple addition of 99TcmO4 from a commercial generator diluted in a buffer. The most suitable buffer was found to be isotonic citrate/saline at pH 9.0 to 9.5. When the kits are prepared as described and reconstituted with the above buffer, labelling yields of more than 95% are routinely achieved and polymerization or stacking of the labelled compounds is prevented.
A patient is described in whom two different sites of cannulation of central veins produced markedly different pressures with potentially dangerous consequences. Falsely elevated pressures recorded from a catheter inserted via the subclavian vein were related to the patency in the arm of an arteriovenous shunt. The likely cause of this phenomenon is discussed.
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The anatomy and physiology of the pulmonary epithelial barrier are briefly described, and methods of measuring permeability of the barrier to solutes are outlined, including findings on alveolar barrier permeability to 99mTcDTPA. A method for measuring permeability to 99mTcDTPA of the conducting airways is described in which the effect of mucociliary clearance can be quantified using radio-labelled polystyrene microspheres 5 mum in diameter. When the 99mTcDTPA clearance rates from inner, intermediate and outer zones of the lungs are corrected fro the effect of mucociliary clearance, there is a significantly slower clearance from the conducting airways than from the alveoli.
Vasoactive intestinal peptide causes bronchodilatation when given intravenously but is less effective in both animals and man when given by inhalation. This difference may be due to poor transit of the peptide across the bronchial epithelium. To test this hypothesis pulmonary clearance of radiolabelled vasoactive intestinal peptide was measured in Sprague Dawley rats and compared with that of pertechnetate (TcO4-) and diethylene triamine pentaacetate (DTPA). Despite a molecular weight (MW) of 3450, iodinated vasoactive intestinal peptide was cleared rapidly from the lungs, with a mean half time (t1/2) of 19 minutes after an initial slower phase. This compares with a t1/2 of 10 minutes with TcO4- (MW 163) and a t1/2 of 158 minutes with DTPA (MW 492). The possibility that vasoactive intestinal peptide mediates a non-specific increase in permeability was discounted by the fact that the combination of vasoactive intestinal peptide and DTPA did not alter DTPA clearance significantly. Chromatography and radioimmunoassay of blood taken after intratracheal administration of vasoactive intestinal peptide demonstrated a metabolite but no unchanged peptide. An intravenous injection of the peptide disappeared on first pass through the lung. It is concluded that inhaled vasoactive intestinal peptide lacks efficacy as a bronchodilator not because of slow diffusion to airway smooth muscle but because it is metabolised at an early stage of its passage through the respiratory epithelium.
This case report describes a patient who sustained a laceration of the hepatic artery during external cardiac massage, a complication which has not previously been reported. The spleen was also damaged. The importance of recognising complications such as haemorrhage from injured abdominal viscera is emphasised and the literature relating to these injuries is briefly reviewed.