Arterial Blood Gas Tensions Research Articles

Effect of body position on gas exchange in patients with unilateral pleural effusion: influence of effusion volume

The objective of this study was to evaluate the effect of lateral body position on gas exchange in patients with unilateral pleural effusion, with special reference to the influence of effusion volume. Thirty consecutive patients with unilateral pleural effusion, without evidence of parenchymal pulmonary involvement, were entered into the study. Arterial blood gas tensions ( PaO 2, PaCO 2) were randomly measured in both right and left lateral decubitus body positions, while breathing room air. To assess the influence of the effusion volume, roentgenographic and functional parameters were used. Among the latter, FVC, FEV 1, TLC and RV were determined. The influence of the presence or absence of pleuritic pain on gas exchange was also assessed. There was no significant difference in PaCO 2 between right and left lateral decubitus body positions (31·1 ± 4·2 vs. 31·0 ± 4·5 mmHg). The differences in PaO 2 between the two body positions ranged from 0·5–2·5 mmHg (mean 9·3 ± 6·6 mmHg). Mean PaO 2 with the normal-side (control) down ( PaO 2-N) (81·4 ± 8·5 mmHg) was higher, but without significant statistical difference, than mean PaO 2 with the effusion-side down ( PaO 2-E) (78·0 ± 12·5 mmHg). PaO 2-N was higher than PaO 2-E in 22 of 30 patients (conventional), and lower in eight patients (paradoxical). No consistent relationship was found for alterations in PaO 2 in different positions with the volume of effusion, either when estimated by a roentgenographic method or when using spirometric or plethysmographic values. The mean difference between PaO 2 values in the two positions ( ΔPaO 2 N-E) (6·3 ± 9·8 mmHg) in patients with chest pain was significantly greater ( P<0·05) than the ΔPaO 2 N-E in patients without pain (−3·3 ± 10·7 mmHg). Moreover, only pleuritic chest pain showed a significant statistical influence on ΔPaO 2 N-E, when all factors were analysed simultaneously. Although gas exchange is improved in most patients in the lateral decubitus position with normal-side down, some patients behave paradoxically. This difference does not appear to be related to the effusion volume, but seems to be influenced by the presence of pleural pain.

Cardiovascular effects of epidurally administered morphine and a xylazine-morphine combination in isoflurane-anesthetized dogs

Abstract Cardiovascular effects of epidurally administered morphine, a morphine-xylazine combination, and saline solution (control) during isoflurane-maintained anesthesia were assessed in 6 healthy dogs. Anesthesia was induced with isoflurane in O2 and was maintained at 2.0% end-tidal isoflurane concentration. Ventilation was controlled to maintain PaCO2 at 35 to 45 mm of Hg. The dorsal pedal artery was cannulated for measurement of systolic, mean, and diastolic pressures, and for blood sample collection. Arterial blood pH and gas tensions were determined every 30 minutes. Cardiac output was determined by thermodilution. The ecg, heart rate, body temperature, central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, end-tidal isoflurane concentration, and CO2 tension were monitored. Systemic and pulmonary vascular resistance, arterial HCO3- concentration, base excess, and cardiac index were calculated. After baseline measurements were taken, morphine (0.1 mg/kg of body weight) in 5 ml of isotonic saline solution, morphine and xylazine (0.1 mg of morphine and 0.02 mg of xylazine/kg) in 5 ml of isotonic saline solution, or 5 ml of isotonic saline solution was injected into the lumbosacral epidural space. Data were recorded at 5, 15, 30, 45, 60, 75, 90, 105, and 120 minutes after epidural injection. Statistical analysis included anova for repeated measures. Significance was set at P &lt; 0.05. None of the measured variables was significantly different among the 3 treatments at any time. Results of the study indicated that epidural administration of morphine or morphine and xylazine is not associated with significant cardiovascular side effects during isoflurane-maintained anesthesia in dogs.

Effect of protriptyline, 10 mg daily, on chronic hypoxaemia in chronic obstructive pulmonary disease

A daily dose of 20 mg of protriptyline can improve daytime arterial blood gas tensions in chronic obstructive pulmonary disease (COPD). Its usefulness is limited by anticholinergic side-effects. This study examined whether a daily dose of 10 mg of protriptyline improved daytime arterial oxygen tension (PaO2) and quality of life in patients with stable mild or moderate hypoxaemia caused by COPD. Twenty six patients were randomized to receive protriptyline or placebo in a double-blind parallel-group trial for 12 weeks, following a run-in period of 4 weeks, in order to assess the stability of hypoxaemia. Patients with a change in PaO2 of > 0.7 kPa during the run-in were excluded. Spirometry, quality of life and dyspnoea score were measured at randomization and after 12 weeks, whilst arterial blood gas tensions were also measured 2 and 6 weeks after randomization. No improvement in arterial blood gas tensions, spirometry values, dyspnoea score, or quality of life was found in either the protriptyline or the placebo group. The majority of patients receiving protriptyline experienced anticholinergic side-effects, which necessitated the withdrawal of the drug in one patient. We conclude that there was no evidence that a daily dose of 10 mg of protriptyline had a significant effect on daytime arterial oxygen tension in stable mild and moderate hypoxaemia caused by COPD. Despite the low dose, anticholinergic side-effects occurred in most patients.

Effects of Body Position, Hyperinflation, and Blood Gas Tensions on Maximal Respiratory Pressures in Patients with Chronic Obstructive Pulmonary Disease

BACKGROUND--Inspiratory muscle strength in patients with chronic obstructive pulmonary disease (COPD) can be affected by mechanical factors which influence the length of the diaphragm, and by non-mechanical factors. The aim of the present study was to evaluate firstly the effects of body position on respiratory pressures and, secondly, to determine the relative contribution of age, body mass index (BMI), lung volumes, and arterial blood gas tensions to respiratory muscle strength. METHODS--Thirty male patients with stable COPD (mean FEV1 40.4% predicted) participated in the study. Maximal inspiratory and expiratory mouth pressures (PImax, PEmax) and maximal inspiratory transdiaphragmatic pressures (PDI) in the sitting and supine position, lung function, and arterial blood gas tensions were measured. RESULTS--Mean (SD) PImax in the sitting position was higher than in the supine position (7.1(2.3)kPa v 6.4(2.2)kPa respectively). In contrast, PDI in the sitting position was lower than in the supine position (10.0(3.5)kPa v 10.8(3.7)kPa respectively). PEmax was higher in the sitting position (9.3(3.0)kPa) than in the supine position (8.7(2.8)kPa). Significant correlations were found between inspiratory muscle strength on the one hand, and lung function parameters, BMI, and arterial blood gas tensions on the other. CONCLUSIONS--Inspiratory muscle strength in patients with COPD is influenced by mechanical factors (body position, lung volumes) and non-mechanical factors (BMI, FEV1, and blood gases). PImax and PEmax are lower in the supine position while, in contrast to healthy subjects, PDI is higher in the supine position than in the sitting position.

Arterial blood gas analysis or oxygen saturation in the assessment of acute asthma?

A study was undertaken to determine if arterial blood gas estimation is always necessary in the assessment of patients presenting to hospital with acute severe asthma, or whether oxygen saturation as measured by pulse oximetry is a reliable screening test for predicting those in respiratory failure. A prospective study was conducted in a specialist respiratory medical unit. Arterial blood gas tensions and pulse oximetry were measured in 89 consecutive patients admitted with acute severe asthma. Respiratory failure was defined as PaO2 < 8.0 kPa or PaCO2 > 6 kPa. When oxygen saturation was 92% or higher (72 patients) respiratory failure was found in three (4.2%) cases. In the 82 patients with a saturation of 90% or higher six patients (7.3%) had respiratory failure. In the initial assessment of acute severe asthma an oxygen saturation of > 92% suggests that respiratory failure is unlikely and therefore arterial blood gas measurement is unnecessary. This study is only relevant to the assessment of asthmatic patients at presentation. Other parameters of severity must be continually assessed in all asthmatic patients admitted to hospital irrespective of the initial SaO2, and blood gases measured when clinically indicated.

Effect of inhibition of prostaglandin synthesis on breathing movements and pulmonary blood flow in fetal sheep

During transition from fetal to extrauterine life, respiration increases in incidence and magnitude as pulmonary blood flow dramatically increases. To determine whether alterations in pulmonary blood flow in utero are directly related to alterations in fetal breathing movements (FBM), we studied six chronically instrumented fetal sheep late in gestation to assess the effects of continuous FBM caused by a 4-h infusion of meclofenamate, a prostaglandin synthase inhibitor, on mean pulmonary blood flow to the fetus. We found a striking increase in FBM from 46 +/- 15% (SD) of the time during control to > 85% of the time by 1 h (P < 0.001), with the fetuses exhibiting continuous FBM by the last 1 h of infusion. The mean pulmonary blood flow also increased significantly during the first 90 min of the infusion as the incidences of FBM were increasing (26 +/- 14 and 56 +/- 23 ml.min-1.kg-1 for control and infusion, respectively; P < 0.01). Despite the simultaneous initial increase in FBM and mean pulmonary blood flow, the increase in left pulmonary artery blood flow was not sustained and decreased back to baseline by 2 h, even though the incidence of FBM continued to increase at this time. During the infusion, the mean pulmonary blood flow was not different between the presence or absence of FBM. There were no changes in fetal heart rate or pulmonary or systemic blood pressures during the infusion nor in arterial pH or blood gas tensions. We conclude that this increase in mean pulmonary blood flow in utero was not solely related to the increase in breathing movements.

Post-ischemic hyperemia in the cat retina: the effects of adenosine receptor blockade.

Significant hyperemia results after 1 h of retinal ischemia in cats. Adenosine receptor blockade significantly attenuates the increase in retinal blood flow that occurs in response to systemic hypoxia. Synthesizing these findings, I hypothesized that adenosine receptor antagonism would attenuate the increase in blood flow that follows retinal ischemia. In these experiments, blood flows were measured with radioactively labeled microspheres in the retina and choroid of adult cats anesthetized with chloralose and acepromazine. Ischemia was induced for 1 h in both eyes by elevation of intraocular pressure above systolic arterial pressure. Blood flows were measured before ischemia and 5 min after the return of normal intraocular pressure. In each animal, after baseline blood flows were determined and approximately 10-15 min before ischemia was induced, one eye received 0.1 ml of intravitreal 0.01M 8-sulfophenyltheophylline, a polar adenosine receptor antagonist, while the opposite eye, the control, received an equal volume of intravitreal saline. Arterial blood gas tensions, systemic arterial pressure, hematocrit, and anesthetic level were kept constant during the experimental protocol. Compared with control eyes, hyperemia was significantly attenuated in the retinal circulation after ischemia in eyes injected with 8-sulfophenyltheophylline. Increase in post-ischemic choroidal blood flow was not affected. Although adenosine is involved in the vasodilatation that occurs when blood flow is restored after retinal ischemia, adenosine receptor blockade did not completely abolish hyperemia, implying that blockade was incomplete or other vasoactive substances also affect post ischemic hyperemia in the retina.

Nasal ventilation in acute exacerbations of chronic obstructive pulmonary disease: effect of ventilator mode on arterial blood gas tensions.

There are no controlled trials of the use of different modes of nasal intermittent positive pressure ventilation (NIPPV) in patients with exacerbations of chronic obstructive pulmonary disease (COPD). This study describes the effect on blood gas tensions of four different modes of nasal ventilation. Twelve patients with acute exacerbations of COPD were studied (mean (SD) FEV1 0.59 (0.13) l, PaO2 (air) 5.10 (1.12) kPa, PaCO2 9.28 (1.97) kPa, pH 7.32 (0.03)). Each patient underwent four one-hour periods of nasal ventilation in randomised order: (a) inspiratory pressure support 18 cm H2O; (b) pressure support 18 cm H2O+positive end expiratory pressure (PEEP) 6 cm H2O (IPAP+EPAP); (c) continuous positive airway pressure (CPAP) 8 cm H2O; and (d) volume cycled NIPPV. Arterial blood samples were obtained before each period of ventilation and at one hour. Pressure support, CPAP, and volume cycled NIPPV all produced significant improvements in PaO2; there was no difference between these three modes. The change in PaO2 with IPAP+EPAP did not reach statistical significance. None of the modes produced significant changes in mean PaCO2; patients with higher baseline levels tended to show a rise in PaCO2 whereas those with lower baseline levels tended to show a fall. Although PaO2 improved in all patients there are differences in efficacy between the modes, while the changes in PaCO2 were variable. The addition of EPAP conferred no advantage in terms of blood gas tensions.

Minimum Alveolar Concentration for Halothane in the Rat Is Resistant to Effects of Forebrain Ischemia and Reperfusion

Because glutamate antagonists can substantially alter the minimum alveolar concentration (MAC) of volatile anesthetics, glutamate has been implicated as an important neurotransmitter in processes contributing to the anesthetic state. Cerebral ischemia profoundly alters glutamatergic neurotransmission and thus may also alter halothane MAC. Fasted rats were surgically prepared for forebrain ischemia. One half of the animals served as operative shams (n = 24). Remaining rats underwent 10 min of bilateral carotid occlusion combined with systemic hypotension (n = 24). In animals in both groups brain circulation was restored for 1 h, 24 h, or 7 days (n = 8). At each of these intervals, MAC for halothane was determined by the tail-clamp method. Histologic damage in the hippocampus, cortex, caudoputamen, and thalamus was measured in animals allowed to survive 7 days. Blood pressure, arterial blood gas tensions and pH, pericranial temperature, and plasma glucose values measured immediately before ischemia were similar among groups. Neither ischemia nor duration of reperfusion significantly altered halothane MAC as compared with operative shams (sham 1 h = 0.9 +/- 0.1 vol%, 24 h = 1.0 +/- 0.1 vol%, 7 days = 1.0 +/- 0.2 vol%; ischemia 1 h = 0.9 +/- 0.1 vol%, 24 h = 0.9 +/- 0.1 vol%, 7 days = 1.0 +/- 0.2 vol%). Histologic damage in the hippocampus and caudoputamen was severe in the ischemic group of animals. Mild injury was observed in the motor and cingulate cortex as well as the thalamus. There was no evidence of histologic injury in sham-operated animals. The absence of effect of ischemic forebrain injury on halothane MAC is consistent with findings made in other models of supratentorial cerebral injury. These results support the contention that anatomic foci for motor responses elicited during MAC determination are localized at levels caudal to the forebrain.

Long term non-invasive domiciliary assisted ventilation for respiratory failure following thoracoplasty.

Ventilatory failure is a well recognised complication of patients who have had a thoracoplasty for tuberculosis, but there are few data regarding the value of long term non-invasive assisted ventilation in this situation. Thirty two patients who had had a thoracoplasty 20-46 years previously and who had developed respiratory failure were treated with nocturnal cuirass assisted ventilation or nasal positive pressure ventilation. Their survival and changes in arterial blood gases, nocturnal oximetry, and pulmonary function tests were assessed. The actuarial survival rates at one, three, five, and seven years after starting treatment were 91%, 74%, 64%, and 55%, respectively. Only seven of the 13 deaths were directly attributable to chronic respiratory or cardiac failure. The arterial PO2, PCO2, mean nocturnal oxygen saturation, vital capacity, and maximal inspiratory and expiratory pressures had all improved at the time of the initial post-treatment assessment (mean 12 days after starting treatment), but no subsequent improvements were seen after up to 48 months of follow up. Neither survival nor physiological improvements were correlated with the patients' age, the interval since thoracoplasty, or the pretreatment arterial blood gas tensions or results of pulmonary function tests. These results show that, even when ventilatory failure has developed, the prognosis with non-invasive assisted ventilation is good and the physiological abnormalities can be partially reversed. Patients who develop respiratory failure after a thoracoplasty should be considered for this type of long term domiciliary treatment.

Peripheral and Central Chemoreceptor Control of Ventilation During Exercise in Humans

The stability of arterial blood gas tensions and pH during steady-state moderate exercise has suggested an important humoral element of ventilatory control in humans. However, the involvement of central and peripheral chemoreflexes in this humoral control remains controversial. This reflects, in large part, technical and interpretational limitations inherent in currently used estimators of chemoreflex "sensitivity." Evidence suggests that the central chemoreceptors (a) contribute little during moderate exercise, given the relative stability of cerebrospinal pH, (b) constrain the hyperpnea of high-intensity exercise, consequent to the respiratory compensation for the metabolic acidemia, and (c) may play a role in the respiratory compensation during chronic metabolic acidemia. In contrast, the peripheral chemoreceptors appear to (a) exert considerable influence on ventilatory kinetics in moderate exercise, but are less important in the steady state, and (b) induce much of the respiratory compensation of high-intensity exercise.

Hyperbaric oxygenation increases arousal and breathing movements in fetal lambs

Oxygenation produced by distending the lungs with 100% O2 increases the occurrence of arousal and fetal breathing movements (FBM), particularly during non-rapid-eye-movement (NREM) sleep, in fetal sheep of > or = 135 days of gestation. We studied the breathing and behavioral responses to a rise in arterial PO2 (PaO2) without lung distension in fetuses between 128 and 132 days of gestation. Twelve fetuses were chronically instrumented to record FBM, behavioral state, blood pressure, arterial blood gas tensions, and pH. Fetal PaO2 was raised by having the ewe breathe 100% O2 at 3 atmosphere absolute pressure spontaneously (group 1, n = 5, 129 +/- 1 days of gestation) or with mechanical ventilation to control fetal arterial PCO2 (group 2, n = 7, 131 +/- 1 days of gestation). Hyperbaric oxygenation raised fetal PaO2 by 20 Torr in both groups. During hyperbaric oxygenation, the occurrence of arousal increased severalfold in both groups. The occurrence of FBM increased during arousal in both groups, during rapid-eye-movement sleep in group 1, and during NREM sleep in group 2. The timing of diaphragmatic activity during arousal and the variability of diaphragmatic activity during NREM sleep were different than those in rapid-eye-movement sleep. We conclude that oxygenation without lung distension increases the occurrence of arousal and of FBM, principally during arousal and NREM sleep, in fetuses of < or = 135 days of gestation.

Cardiovascular effects of periodic obstructive and central apneas in dogs.

Patients with sleep apnea may experience two types of apnea, central and obstructive. We compared cardiovascular effects of these two types of apnea matched for changes in arterial blood gas tensions and periodicity. In 12 anesthetized, closed chest dogs, obstructive apneas were induced by completely occluding the endotracheal tube at end-expiration for 1 min and allowing 1 min of spontaneous ventilation. Central apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on with the same periodicity as obstructive apneas. During both types of apnea, changes in arterial PO2 and PCO2 were approximately the same. During obstructive apneas, mean blood pressure (BP) and cardiac output (CO) did not change significantly, heart rate (HR) decreased by 27% (p < 0.001), and stroke volume increased by 7.8 ml (p < 0.005). During central apnea, BP did not change, but HR and CO decreased by far more than with obstructive apneas: 44% (p < 0.001) and 27% (p < 0.05) respectively, and stroke volume increased by 5.0 ml (p < 0.05). During obstructive apneas, right atrial pressure increased, as did right heart blood volume. During central apneas, both right atrial pressure and left atrial pressure increased, as did pulmonary blood volume. We conclude that: (1) HR decreases are more severe during central apnea, most likely due to lack of respiratory mechanoreceptor input; (2) CO decreases more with central compared with obstructive apnea due to the heart rate response; (3) HR-induced cardiac dysfunction with central apnea could lead to pulmonary vascular congestion.

Effects of body position, hyperinflation, and blood gas tensions on maximal respiratory pressures in patients with chronic obstructive pulmonary disease.

Inspiratory muscle strength in patients with chronic obstructive pulmonary disease (COPD) can be affected by mechanical factors which influence the length of the diaphragm, and by non-mechanical factors. The aim of the present study was to evaluate firstly the effects of body position on respiratory pressures and, secondly, to determine the relative contribution of age, body mass index (BMI), lung volumes, and arterial blood gas tensions to respiratory muscle strength. Thirty male patients with stable COPD (mean FEV1 40.4% predicted) participated in the study. Maximal inspiratory and expiratory mouth pressures (PImax, PEmax) and maximal inspiratory transdiaphragmatic pressures (PDI) in the sitting and supine position, lung function, and arterial blood gas tensions were measured. Mean (SD) PImax in the sitting position was higher than in the supine position (7.1(2.3)kPa v 6.4(2.2)kPa respectively). In contrast, PDI in the sitting position was lower than in the supine position (10.0(3.5)kPa v 10.8(3.7)kPa respectively). PEmax was higher in the sitting position (9.3(3.0)kPa) than in the supine position (8.7(2.8)kPa). Significant correlations were found between inspiratory muscle strength on the one hand, and lung function parameters, BMI, and arterial blood gas tensions on the other. Inspiratory muscle strength in patients with COPD is influenced by mechanical factors (body position, lung volumes) and non-mechanical factors (BMI, FEV1, and blood gases). PImax and PEmax are lower in the supine position while, in contrast to healthy subjects, PDI is higher in the supine position than in the sitting position.

IgE level in blood serum in patients with pollinosis

We operated on 14 singleton fetal sheep at 126 +/- 3 d gestation and produced nonimmune anemia in 12 of them to study the mechanisms responsible for hydrops. Two fetuses served as controls. Partial exchange transfusions were performed daily to lower the hematocrit while we measured arterial blood gas tensions; Hb concentration; oxygen saturation; arterial oxygen content; aortic, central venous, and umbilical venous pressures; heart rate; plasma protein concentration; and colloid osmotic pressure. Hydrops developed in six of the fetuses and did not develop in six others, although both groups were anemic to the same degree, had similar total amounts of blood withdrawn based on kilograms of dry weight, and had similar dry weights. The fetuses who had hydrops became anemic more rapidly than the nonhydropic fetus (5.2 +/- 1.9 versus 8.3 +/- 2.7 d; p < 0.05) and had more blood exchanged each day (197 +/- 56 versus 113 +/- 28 mL/kg dry body wt/d; p = 0.008). Umbilical venous pressures increased in both hydropic and nonhydropic fetuses, but the central venous pressure became elevated only in the hydropic fetuses. Changes in heart rate, arterial pH and blood gas tensions, arterial oxygen content, plasma protein concentration, colloid osmotic pressure, and aortic pressure were similar in both groups. At autopsy the hydropic fetuses had 78 +/- 47 mL of ascites and 20 +/- 26 mL of pleural fluid. The water content of the hydropic fetuses and of the hydropic fetuses' placentas was greater than that of the nonhydropic fetuses. We conclude that a more rapid development of anemia is associated with hydrops in fetal sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional cerebral blood flow during submergence asphyxia in Pekin duck

The cerebrovascular response to submergence asphyxia was studied in the Pekin duck (Anas platyrhynchos var.) by use of the cerebral blood flow (CBF) tracer [14C]isopropyliodoamphetamine and quantitative autoradiography. Blood flow of the whole brain was 158 +/- 14 (SE) ml.min-1 x 100 g-1 (n = 7) in control animals. There was a doubling of flow to 320 +/- 61 ml.min-1 x 100 g-1 (n = 6) during submergence asphyxia. The hypothesis that CBF is redistributed within the brain during asphyxia was not supported. There were no regional reductions in CBF during submergence asphyxia. Mean arterial blood pressure was similar (approximately 140 mmHg), but heart rate, arterial blood gas tensions, and arterial pH were significantly different in control and submerged ducks at the time CBF was measured. The differences in CBF among submerged animals correlated strongly with arterial PCO2 and mean arterial blood pressure. The smallest proportional difference in regional CBF between control and submerged ducks occurred in the ectostriatum (+141%) and the largest in the locus ceruleus (+241%). The largest absolute difference in regional CBF was in the nucleus ruber (+322 ml.min-1 x 100 g-1). These are the first measurements of blood flow in discrete nuclei and regions of the avian brain.

Marital status and sexual adjustment after colectomy. Results in 178 patients operated on for ulcerative colitis.

The frequency of marriage and divorce did not differ from that of the general population. Female ileostomists married less often than females with ileorectal anastomosis (IRA) and had reduced fertility. Genital functional disturbance was not reported by the IRA males but occurred in 8 of 52 male ileostomists below 50. The coital activity, however, seemed undisturbed except for one married male. Dyspareunia was experienced by 8 of 15 IRA females aged 16-49 and intercourse triggered precipitancy in 2 of them. In a similar group of ileostomists only 5 of 50 had occasional dyspareunia. The coital practice and frequency in married patients did not seem to differ from a general population. Premarital activity seemed low in ileostomists of either sex. This as well as the low marriage rate in females may be ascribed to the psychological effects of a stoma and an appliance with contents.

Identification of peripheral chemoreceptor stimuli

This short review considers the essential structure and stimulus-response characteristics of the carotid body chemoreceptors and attempts to relate the latter to their role in the generation of exercise hyperpnea. It shows that the arterial chemoreceptors do contribute substantially to the drive to breathe in exercising man and it suggests that this extra drive results from an increase in discharge which occurs in spite of the fact that the classical stimuli to its discharge, do not change. The possibility that in exercise the carotid body is excited by activation of its sympathetic innervation, and by raised arterial potassium, is considered. The idea that breath-by-breath oscillations of arterial blood gas tension convey accurate information about the whole body rate of carbon dioxide production is described and found wanting.

The Effect of Exogenous Surfactant Therapy on Lung Function Following Cardiopulmonary Bypass

Pilot study to investigate the effect of exogenous surfactant therapy on lung function following cardiopulmonary bypass (CPB). Prospective randomized controlled study. Adult intensive care unit of a postgraduate cardiothoracic hospital. Sixteen adult patients undergoing elective coronary artery revascularization surgery without a history of preoperative respiratory disease. Artificial lung-expanding compound (ALEC, Britannia Pharmaceuticals, Crawley, UK) 3.2 g, was given via a bronchoscope 60 min after bypass in eight patients. Eight control subjects received air. Lung function tests during IPPV (arterial blood gas tensions, Crs, FRC, TLco, KCO) were measured prior to CPB, before therapy, and at regular intervals up to 180 min afterwards. The CPB caused a significant impairment of lung function in both groups with an increase in A-a gradient (+47 +/- 11 mm Hg in the ALEC group and +44 +/- 17 mm Hg in controls) and reductions in FRC (-290 +/- 121 ml in the ALEC group and -470 +/- 132 ml in controls), TLco (-1.6 +/- 0.3 ml/min/mm Hg in the ALEC group and -2.2 +/- 0.3 ml/min/mm Hg in controls), and Crs (-10 +/- 1 ml/cm H2O in the ALEC group and -21 +/- 4 ml/cm H2O in controls). The ALEC therapy did not affect A-a gradient, FRC, and Crs compared with controls. However, TLco was significantly lower in the ALEC group following therapy (120 min after treatment -0.1 +/- 0.3 ml/min/mm Hg in ALEC group and +1.0 +/- 0.3 ml/min/mm Hg in controls). A single 3.2-g dose of ALEC administered as a bolus bronchoscopically does not improve lung function following CPB and may impair gas transfer.

Carbamazepine‐induced pneumonitis

To present a case of a rare pulmonary reaction to carbamazepine. One month after starting carbamazepine therapy, a previously well 38-year-old man developed pulmonary interstitial pneumonitis associated with debilitating systemic symptoms, the cause of which was not diagnosed for a further three months. Transbronchial lung biopsy showed granulomatous inflammation consistent with an allergic drug reaction. The patient's clinical status, chest x-ray appearance and arterial blood gas tensions all normalised after withdrawal of the drug without any specific therapy. Pneumonitis is a rare adverse reaction to carbamazepine therapy. However, awareness may reduce delays in both diagnosis and withdrawal of the drug.