On-line deadspace measurement during cardiac surgery.
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Biomedical subjects
Publications and source records attributed to R Fletcher.
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Cyclic nucleotide metabolism was examined in the retina and in the retinal pigment epithelium (RPE)-choroid complex of the rds mouse (020/A), a mutant in which discrete photoreceptor outer segment disc structures fail to develop. In retinas of both rds and control (Balb/c) mice, cyclic AMP levels peak at 10-15 days (20-25 pmol mg-1 protein). The level drops to about 10 pmol mg-1 at about one month in normal retinas but remains high in affected retinas. Cyclic GMP levels increase five-fold in Balb/c retinas as ROS develop whereas, in affected retinas, the levels remain constant and low (about 5 pmol mg-1). In RPE-choroid, cyclic nucleotide levels are similar in control and affected mice. Cyclic AMP phosphodiesterase (PDE) activity is somewhat higher in affected than in control retinas; conversely, cyclic GMP-PDE is lower. Both cyclic AMP-PDE and cyclic GMP-PDE activities are different in normal and affected RPE-choroid. Thus, although the rds (020/A) mouse belongs to the early-onset photoreceptor dysplasia group of hereditary retinal degenerations on a morphological basis, it does not exhibit high retinal cyclic GMP levels and thus appears to be distinct from other animals exhibiting early postnatal photoreceptor dysfunction.
Units for the investigation of susceptibility to malignant hyperthermia (MH) were set up in Denmark in 1977 and in Sweden in 1981. Two hundred and ten patients from 76 families have been investigated. The diagnosis of MH susceptibility (MHS) was made by in vitro exposure of muscle from vastus medialis to halothane and to caffeine. MHS criteria for the patients in this paper were established from examination of 31 control biopsies, obtained from the same muscle and with the same anaesthesia as the MH patients. The criteria have since been changed to those presented elsewhere in this issue. In our laboratories the halothane test (exposure to 0.5-2% halothane) was the more sensitive: 88% of MHS patients reacted to it. The caffeine test was positive in 68% of MHS patients, 0.5-2.0 mmol litre-1 solutions being the most discriminating. Forty-two percent of MHS patients reacted to only one test. Fulminant MH was the most common reason for investigation; all these families contained MHS members. Masseter spasm occurred as sole sign in 21 families, of which 11 were MHS. Only 10% of MHS patients had other signs or symptoms of neuromuscular disease such as muscle cramps or muscular dystrophy. Three families had experienced sudden infant death syndrome (SIDS), and two teenage brothers in a MHS family died suddenly, but death was unrelated to anaesthesia.
Using the single breath test for carbon dioxide (SBT-CO2), the components of physiological deadspace were investigated during anaesthesia with IPPV in 58 patients. A square-wave inspiratory flow and an end-inspiratory pause (25% and 10% of cycle time, respectively) were used. At tidal volumes of 0.45 litre (f = 17 b.p.m.), and 0.75 litre (f = 9 b.p.m.), median values for VDphys/VT were 0.44 and 0.31. Increasing VT and decreasing f did not change airway deadspace (VDaw) so that the fraction VDaw/VT was decreased (P less than 0.001). The alveolar deadspace fraction, VDalv/VTalv, was decreased in 93% of patients (P less than 0.001). These improvements with increasing VT can be attributed to beneficial effects on gas distribution and diffusion time. Patients with large alveolar deadspaces had steeply sloping SBT-CO2 phase III, and increased expiratory time constants of the respiratory system. The median arterial--end-tidal PCO2 difference, (PaCO2-PE'CO2), was 0.6 kPa at small and 0.3 kPa at large tidal volumes (P less than 0.001). Three patients had zero and four had negative (PaCO2-PE'CO2) values at large tidal volumes. When phase III slopes steeply, negative (PaCO2-PE'CO2) values may be observed in the presence of alveolar deadspace.
The aim of this study was to observe the effects of the position of the tracheal tube on cardiac performance or sedation requirements after cardiac surgery. There were no significant differences in heart rate, systolic blood pressure, or rate-pressure product during the first 16 hours postoperatively when 41 orally intubated patients were compared with 32 patients who were reintubated nasally. The two groups received similar amounts of sedative drugs postoperatively. During attempted nasal intubation, bleeding developed in four patients, and in three of these and four others the tube could not be passed. Failed nasal intubation gave rise to nasal discomfort in three of seven patients. Orally intubated patients complained more often of sore throat after extubation, whereas those who had been nasally intubated complained of discomfort in the nose and throat. We conclude that nasal re-intubation carries no advantage over oral intubation for ventilation after cardiac surgery.
In order to calculate alveolar deadspace, an important measure of ventilation/perfusion mismatching, it is necessary to measure airway or anatomical deadspace (VDaw) and physiological deadspace. VDaw is usually measured graphically or by similar means, but sometimes it is estimated from a formula, based on Christian Bohr's work, in which end-tidal PCO2 is used as a measure of alveolar PCO2. In 58 patients undergoing anaesthesia and positive pressure ventilation, there were large errors in this estimate of VDaw compared to a graphical method. At tidal volumes of 400-500 ml, the median error was 34 ml; at larger tidal volumes, the median error increased to 74 ml (P less than 0.001). The size of the error was correlated to the slope of phase III, the part of the CO2 tracing representing alveolar CO2, at both ventilator settings (P less than 0.01). It is concluded that estimates of VDaw based on end-tidal PCO2 are unreliable, and their use will lead to a large part of the alveolar deadspace being wrongly accredited to VDaw.
The NASPE Mode Code Committee was formed in response to the growing need for efficient means of describing the function of increasingly complex single- and dual-chamber cardiac pacemakers. After considering numeric, alphabetic, and pictorial codes, the Committee recommended the adoption of two codes: a generic code which is similar to the Revised ICHD Code and is suitable for conversational use, and a specific code, based on one developed by Brownlee and others, that permits more detailed specification of both antibradycardia and antitachycardia functions. The specific code described in this report was adopted by the NASPE Executive Advisory Committee as the NASPE Specific Code in March, 1983. The generic code was not adopted but is described herein for future reference in the light of experience to be gained in the use of the recently published Revised ICHD Code.
Sixteen patients with diuretic-induced hypokalemia underwent 24-hour ambulatory electrocardiographic monitoring during and after correction of hypokalemia. Plasma potassium averaged 2.83 +/- 0.08 mEq/liter before and 3.73 +/- 0.06 mEq/liter after correction with potassium chloride, triamterene or both. Premature atrial contractions decreased in 6 patients, increased in 6 and remained unchanged in 4. There was no improvement in ventricular ectopic activity after plasma potassium correction. Ventricular ectopic activity improved in 5 patients, worsened in 10 and remained unchanged in 1. Ventricular tachycardia was not observed in either phase. Plasma magnesium remained normal throughout. The investigators conclude that in patients with uncomplicated hypertension, correction of diuretic-induced hypokalemia does not significantly reduce the occurrence of spontaneous atrial or ventricular ectopic activity.
The Siemens-Elema CO2 Analyzer 930 allows calculation of carbon dioxide elimination from the instantaneous measurement of expired gas flow (VE) and carbon dioxide fraction (FECO2). VE is measured in the ventilator and FECO2 at the Y-piece. The most important source of error in the measurement of carbon dioxide elimination is rebreathing, which corresponds to about 24 ml of end-expiratory gas per breath with the standard Y-piece and tubing. This problem may be decreased by the use of non-return valves in the Y-piece. Allowance must be made for the effects of intermolecular interaction between carbon dioxide and the carrier gas, as the reading is about 20% greater with nitrous oxide than with oxygen. This problem can be largely circumvented by calibration with appropriate gas mixtures. Errors resulting from analyser delay are small, and are eliminated completely by the inclusion of fast electronic components. Carbon dioxide analysis is linear with air as carrier gas, but slightly alinear with nitrous oxide in oxygen mixtures. This error can be minimized by using calibration gases with a carbon dioxide content close to that of expired gas. The expiratory flow meter is linear if kept in good condition. Variations in temperature and water content of expired gas cause overestimation of mean expired carbon dioxide fraction (FECO2) by a factor of 1.01-1.02. Compressed gas in the tubing causes a small error which may be neglected at normal airway pressures with tubing of low compliance. Carbon dioxide measurement is slightly affected by barometric pressure. During mechanical ventilation of the lungs in 10 patients with air, FECO2 obtained after corrections for known errors agreed well with Scholander analysis of mixed expired gas.
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Eight hundred twelve men with presumed acute myocardial infarction and left ventricular filling pressure of at least 12 mm Hg participated in a randomized double-blind placebo-controlled trial to assess the efficacy of a 48-hour infusion of sodium nitroprusside. The mortality rates at 21 days (10.4 per cent in the placebo group and 11.5 per cent in the nitroprusside group) and at 13 weeks (19.0 per cent and 17.0 per cent, respectively) were not significantly affected by treatment. The efficacy of nitroprusside was related to the time of treatment: the drug had a deleterious effect in patients whose infusions were started within nine hours of the onset of pain (mortality at 13 weeks, 24.2 per cent vs. 12.7 per cent; P = 0.025) and a beneficial effect in those whose infusions were begun later (mortality at 13 weeks, 14.4 per cent vs. 22.3 per cent; P = 0.04). Nitroprusside should probably not be used routinely in patients with high left ventricular filling pressures after acute myocardial infarction. However, the results in the patients given late treatment suggest that those with persistent pump failure might receive sustained benefit from short-term nitroprusside therapy.
Of 100 consecutive patients of 70 or more years of age who presented for elective surgery, only 27 were considered to lack a medical indication for chest X-ray. Of these 27, 10 patients had abnormal findings on the X-ray. These figures suggest that routine pre-operative chest X-rays in elderly patients are well worthwhile, and that the savings made by abandoning the practice would be more than outweighed by potential delays and disruptions to theatre lists and the loss of relevant information.
An 18-month-old boy with congenital muscular dystrophy began to develop clear signs of the malignant hyperthermia syndrome after 85 min of halothane/nitrous oxide anaesthesia. Dantrolene, 2 mg/kg i.v., was immediately effective, but temperature, heart rate and carbon dioxide production were all increased for 2 days postoperatively in spite of repeated dantrolene administration.
The effects of the cardioselective beta-blockers practolol (Eraldin, ICI) and metoprolol (Seloken, Hässle) were studied during microlaryngoscopy. I. v. practolol (0.4 mg/kg before and 0.2 mg/kg during anaesthesia) did not protect against increases in arterial pressure, although heart rate was reduced. Oral metoprolol (0.2 g for 4 days) reduced the level of arterial pressure both before and during anaesthesia. Variations in arterial pressure were not attenuated. Very low levels of arterial pressure were seen, and variations in arterial pressures were attenuated when metoprolol was combined with fentanyl.