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Biomedical subjects

G Hedenstierna

Publications and source records attributed to G Hedenstierna.

At least 19 recordsLinked to original sources
PubMed1992

Lung function and exposure to asbestos among vehicle mechanics.

Vehicle mechanics (n = 99) exposed to asbestos (annual median value 0.08 f/ml), and local controls (n = 83) not occupationally exposed to asbestos were studied with regard to symptoms and pulmonary function. The inclusion criteria to participate in this study was an age of at least 40 years with no known exposure to lung irritating agents, and for the exposed subjects, more than 15 years occupational exposure to asbestos with at least 20 years from the first exposure. The subjects were studied during identical conditions by means of dynamic and static spirometry, single breath wash-out with nitrogen (N2) and carbon monoxide (CO). The median for cumulative exposure of asbestos during the entire work life among the studied mechanics was 2.3 f*y/ml. The mechanics had reduced transfer factor (TLCO), after adjustment for age, height, and smoking category. A significant dose-response relationship was noted between the cumulative exposure of asbestos and CV%. The findings suggest a slight influence of small airways and alveoli. The evaluation of the prognostic significance of this requires a longitudinal study.

Adult↗
PubMed1992

Atelectasis and lung function in the postoperative period.

Thirteen patients with healthy hearts and lungs, and with a mean age of 68 years, who were scheduled for lower abdominal surgery during isoflurane anaesthesia with muscular paralysis, were investigated with arterial blood gases, spirometry, pulmonary x-ray and computed tomography (CT) of the chest before and during anaesthesia, as well as during the first 4 postoperative days. Before anaesthesia, lung function and gas exchange were normal in all patients. Pulmonary x-ray and CT scans of the lungs were also normal. During anaesthesia, 6 of 13 patients developed atelectasis (mean 1.0% of intrathoracic transverse area in all patients). Two hours postoperatively, 11 of 13 patients had atelectasis and the mean atelectatic area was 1.8%. Pao2 was significantly reduced by 2.1 kPa to 9.8 kPa. On the first postoperative day, the mean atelectasis was unaltered (1.8%). None of the atelectasis found on CT scanning could be detected on standard pulmonary x-ray. Forced vital capacity (FVC) and forced expired volume in 1 s (FEV1) were significantly decreased to 2/3 of preoperative level. Pao2 was significantly reduced to less than 80% of the preoperative level (mean 9.4 kPa). There were significant correlations between the atelectatic area and the impairment in FVC, FEV1, and Pao2. Spirometry and blood gases improved during the succeeding postoperative days, and atelectasis decreased. No patient suffered from pulmonary complications, as judged from clinical criteria and pulmonary x-ray, in contrast to the findings of atelectasis in 85% of the patients by computed tomography.

Abdomen↗
PubMed1992

Influence of hypertonic-hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide. 2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). 3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Oedema formation was terminated by deflating the balloon and reducing the infusion rate. 4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS+furosemide. HHS, 6 ml kg-1, was given as a bolus injection and furosemide, 1 mg kg-1, intravenously as a bolus followed by an infusion of 0.5 mg kg-1 h-1. All dogs were studied for 4 h. 5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant. 6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-1 in groups A, C and D and to 14.7 in group B (only furosemide)). 7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11.0 +/- 5.7; B, 9.7 +/- 3.3; C, 10.5 +/- 3.1 and D, 10.6 +/- 1.8 g kg-1. 8. We speculate that mechanisms other than effective Starling gradients and enhanced diuresis might define a maximal rate of pulmonary oedema clearance.

Animals↗
PubMed1992

Relationships among gas exchange, spirometry and symptoms in asthma.

OBJECTIVES: The severity of asthma is usually evaluated by clinical examination and spirometry. In a small study of asthmatics considerable ventilation/perfusion (VA/Q) inequality was found, however, despite essentially normal flow rates. These findings prompted the current study. METHODS: We prospectively examined symptoms, spirometry and VA/Q inequality in 26 patients with chronic, symptomatic asthma once a week for 9 consecutive weeks. VA/Q measurements were made using a less invasive approach of the multiple inert gas elimination technique and symptoms were scored. RESULTS: Correlation coefficients between indices for VA/Q inequality (log SDQ), spirometry (FEV1.0/VC, MEF25) and symptom scores were only in the range 0.24-0.29. CONCLUSION: We conclude that even at the individual level, symptoms, spirometry and VA/Q inequality are so poorly correlated that one cannot evaluate any of these aspects of asthma without measuring each. The data support the notion that spirometric and gas exchange abnormalities in asthma are caused by different pathophysiologic events.

Asthma↗
PubMed1992

Pulmonary gas exchange response following allergen challenge in patients with allergic asthma.

Pulmonary gas exchange was studied in 8 patients with allergic asthma before and after allergen challenge. Ventilation-perfusion relationships were assessed by the multiple inert gas elimination technique and forced expiratory flow by conventional spirometry. Measurements were made before, 7-8 minutes, and 0.5, 2.5 and 5 hours after challenge. During baseline conditions all patients showed normal forced expiratory flow (FEV1 3.9 +/- 0.77 (SD) l) and gas exchange expressed as the dispersion of pulmonary blood flow, log SDQ (0.35 +/- 0.08), (one of the common descriptors of ventilation-perfusion (VA/Q) inequality). Immediately after challenge there were significant decreases in FEV1 (to 2.3 +/- 0.75 l) and arterial PO2 (from 13.1 +/- 0.9 to 9.5 +/- 1.2 kPa). The developed ventilation-perfusion inequalities were similar to those found in other asthma studies, i.e. mainly a broad (log SDQ increased to 0.73 +/- 0.30) and sometimes bimodal distribution of the perfusion. Thirty minutes after challenge FEV1 significantly improved to 3.2 +/- 1.18 l while log SDQ remained high (0.71 +/- 0.32). Two and a half hours after challenge log SDQ was reduced and almost normalized to 0.38 +/- 0.07. Five patients developed a late phase reaction with decreasing flow rates after 5 hours. Three of these patients also showed increased log SDQ. There was no clear relationship between gas exchange mismatch and reduced forced expiratory flow. The results support the hypothesis that reduced expiratory flow and gas exchange impairment are caused by different pathophysiological mechanisms.

Adolescent↗
PubMed1992

Gas exchange during simulated airway secretion in the anaesthetized rabbit.

We wished to study the effect of airways secretion on gas exchange. Peripheral airway secretion was simulated in 9 rabbits by the continuous inhalation of nebulized isotonic saline, at a droplet size of about 3 microns. Intrapulmonary deposition of saline in the peripheral airways (83% in airways smaller than 0.5 mm) did not alter total inspiratory resistance (mean 5.4 kPa.l-1.s), but led to a decrease in compliance of the total respiratory system from 45.9 to 21.8 ml.kPa-1 after one hour of nebulization. Arterial oxygen tension decreased from 17.8 kPa to 12.1 and 6.9 kPa after 5 and 60 min of nebulization, respectively. PaCO2 was unaffected after 5 min (4.5 kPa) but increased to 7.0 kPa after 60 min of nebulization. Ventilation-perfusion relationships (VA/Q) showed a significant increase in perfusion of areas with low VA/Q ratios (from 0.7 to 6.3% of cardiac output) and in shunt (from 1.4 to 4.3%) after 5 min of nebulization. At the end of the experiment shunt was increased markedly to 29.7% of cardiac output whereas perfusion of low VA/Q regions remained at the same level (7.3%). The results from this animal model indicate that all gas exchange abnormalities known to occur in asthma can be reproduced without measurably increasing the resistance of the respiratory system.

Airway Resistance↗
PubMed1991

Thoracic lymph drainage in the dog: evaluation of a new model.

A new model for selective sampling of thoracic lymph flow (TLF) and abdominal lymph flow (TDA) in the dog was assessed to ascertain whether there were extrathoracic contributions of lymph to the TLF. Inflating a right atrial balloon in 4 dogs and a left atrial balloon in 2 dogs indicated good separation between TLF and TDA. Data on total lymph protein and albumin clearance before and after oleic acid induced pulmonary oedema in an additional 5 dogs indicated that TLF and TDA drained two differing regions. Our data demonstrate that this lymph preparation provides a sample of thoracic lymph flow with no major extrathoracic lymph contamination. We also propose an alternative method to test for extrathoracic contributions to thoracic lymph, by the application of positive end-expiratory pressure, thereby replacing right atrial balloon inflation.

Albumins↗
PubMed1991

Atrial natriuretic peptide in bronchial asthma.

Regulation of ion transport across the airway mucosa may be involved in the mechanisms producing hyperreactivity and asthma. Atrial Natriuretic Peptide (ANP) has been proposed to participate in the pathogenesis of asthma, and it has been found to have a bronchodilatory effect on asthmatic patients. Experimental evidences suggest that ANP also has some effect on fluid accumulation in the lungs. We hypothesise that ANP may also play a role in the pathogenesis of asthma through changes in the transport of water and ions across the airway epithelium.

Animals↗
PubMed1991

Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia.

We have studied the effects of anaesthesia on atelectasis formation and gas exchange in 45 patients of both sexes, smokers and nonsmokers, aged 23-69 yr. None of the patients showed clinical signs of pulmonary disease, and preoperative spirometry was normal. In the awake patient, partial pressure of arterial oxygen (PaO2) decreased with increasing age (P less than 0.001) and the alveolar-arterial oxygen partial pressure difference (PAO2-PaO2) increased with age (P less than 0.001). Shunt, assessed by the multiple inert gas elimination technique, was small (mean 0.5%) and uninfluenced by age. However, there was an increasing dispersion (log SD Q) of ventilation/perfusion ratios (VA/Q) and increasing perfusion of regions of low VA/Q (VA/Q less than 0.1) with increasing age (P less than 0.001 and P less than 0.05, respectively). No patient displayed any atelectasis as assessed by computed x-ray tomography of the chest. During inhalation anaesthesia (halothane or enflurane) with mechanical ventilation, 39 of 45 patients developed atelectasis and shunt. There was a strong correlation between the atelectatic area and the magnitude of shunt (r = 0.81, P less than 0.001). Atelectasis and shunt did not increase significantly with age, whereas log SD Q and perfusion of regions with low VA/Q ratios did (r = 0.55, P less than 0.001 and r = 0.35, P less than 0.05, respectively). Awake, the major determinant of PaO2 was perfusion of regions of low VA/Q ratios, which increased with age. During anaesthesia shunt influenced PaO2 most, low VA/Q being a secondary factor which, however, was increasingly important with increasing age, thus explaining the well-known age-dependent deterioration of arterial oxygenation during anaesthesia.

Adult↗
PubMed1991

Furosemide, when used in combination with positive end-expiratory pressure, facilitates the resorption of extravascular lung water in experimental hydrostatic pulmonary oedema.

The study aimed to establish whether furosemide given intravenously improved resorption of hydrostatic pulmonary oedema in 14 dogs mechanically ventilated with positive end-expiratory pressure (PEEP). Hydrostatic pulmonary oedema was created by simultaneous inflation of a left atrial balloon and rapid intravenous infusion of isotonic saline. The hydrostatic process was terminated by deflating the balloon and reducing the infusion rate. A PEEP of 10 cmH2O (1.0 kPa) was applied in all animals; in seven, furosemide was administered (diuretic group), 1 mg/kg intravenously as a bolus followed by an infusion of 0.5 mg/kg per hour, while the remaining seven dogs served as a control group. All dogs were studied for a period of 4 h. The extravascular lung water measured with the double indicator dilution technique was 28.3 +/- 3.8 (diuretic group) and 28.2 +/- 6.8 ml/kg (control group) during maximum oedema. It was reduced to 16.4 +/- 2.2 (diuretic group) vs 19.8 +/- 3.7 ml/kg (control group) after 4 h of resorption, P less than 0.05. Postmortem gravimetric values of extravascular lung water were 9.1 +/- 3.4 (diuretic group) vs 12.6 +/- 5.0 g/kg (control group). In the diuretic group the urinary output increased threefold, and haemoglobin and serum protein concentrations were higher than in the control group. There was a significantly greater decrease in cardiac output and central blood volume in the diuretic group. In conclusion, furosemide given intravenously improved lung fluid resorption in hydrostatic pulmonary oedema, probably by increasing the plasma colloid osmotic pressure.

Animals↗
PubMed1991

Pulmonary gas exchange correlated to clinical signs and lung pathology in horses with chronic bronchiolitis.

Eight horses (mean weight 438 kg) with chronic obstructive pulmonary disease (COPD) were studied for clinical signs, ventilation/perfusion relationships (VA/Q) and lung morphology. Four horses were killed and necropsied after the study. In horses with COPD, minute ventilation was almost twice as high as normal, whereas PaO2 was significantly decreased. Cardiac output was normal, but pulmonary artery pressure and pulmonary vascular resistance were significantly increased. The VA/Q distribution was abnormal with an increased scatter of VA/Q ratios. However, shunt (VA/Q = 0) was increased in one horse only. Ventilation of dead space and high VA/Q regions (VA/Q greater than 10) were increased markedly and comprised 74 per cent of minute ventilation. On lung biopsy, all horses showed chronic bronchiolitis with epithelial hyperplasia and metaplasia. Diffuse acinar hyperinflation also was evident at necropsy. There was a significant inverse correlation between the respiratory rate and the fractional ventilation of normal VA/Q regions. Also, there was a significant agreement between the extent of bronchiolar epithelial hyperplasia in necropsy specimens of lungs and the degree of ventilation of high VA/Q regions and dead space. The findings suggest that hyperinflation of the lung due to obstructed airways may be the common denominator of increased ventilation of high VA/Q regions and dead space ventilation and of elevated pulmonary artery pressure in horses with COPD from chronic bronchiolitis.

Animals↗
PubMed1991

Does PEEP facilitate the resolution of extravascular lung water after experimental hydrostatic pulmonary oedema?

The effect of mechanical ventilation with positive end-expiratory pressure on the resolution of hydrostatic pulmonary oedema created by temporary left atrial balloon inflation was studied in mechanically ventilated dogs. Immediately after the hydrostatic process was terminated, by deflating the left atrial balloon, the animals were ventilated for 4 h with zero end-expiratory pressure (ZEEP, n = 6) or with a positive end-expiratory pressure (PEEP, n = 6) of 1.0 kPa (10 cmH2O). Gas exchange and extravascular lung water content (EVLW) with the double indicator dilution technique (dye/cold) were studied and gravimetric determination of lung water was made postmortem. EVLW decreased from 31.6 +/- 7.3 mean +/- SD ml.kg.1 during maximal oedema to 14.5 +/- 2.1 ml.kg.1 (p less than 0.001) 4 h after deflation of the left atrial balloon in dogs ventilated with ZEEP. The corresponding values in dogs ventilated with PEEP were a reduction in EVLW from 28.0 +/- 4.1 to 20.7 +/- 4.0 ml.kg.1 (p less than 0.01) (mean decrease 7.3 +/- 4.0 ml.kg.1). EVLW was significantly higher after 4 h on PEEP than after ZEEP (p less than 0.01). Gravimetric values at the end of the experiment were 12.4 +/- 2.8 ml.kg.1 (ZEEP) and 14.7 +/- 4.5 ml.kg.1 (PEEP) (NS). Oxygenation improved in both groups during the resolution of oedema with a more evident and early effect in the PEEP group. It is concluded that mechanical ventilation with PEEP of 1.0 kPa (10 cmH2O) in the resolution phase after experimental hydrostatic oedema improves oxygenation but retards the resolution of oedema.

Animals↗
PubMed1991

Chronic obstructive pulmonary disease and anaesthesia: formation of atelectasis and gas exchange impairment.

Gas exchange impairment and the development of atelectasis during enflurane anaesthesia were studied in 10 patients (mean age 70 yrs) with chronic obstructive pulmonary disease (COPD). Awake, no patient displayed atelectasis as assessed by computed X-ray tomography. The ventilation/perfusion distribution (VA/Q), studied by the multiple inert gas elimination technique, displayed an increased dispersion of VA/Q ratios (the logarithmic standard deviation of the perfusion distribution, mean log Q SD 0.99; upper 95% confidence limit of normal subject: 0.60), and increased perfusion of regions with low VA/Q ratios (0.005 less than VA/Q less than 0.1: 5.4% of cardiac output). Shunt was negligible (mean 0.6%). Computed chest tomography showed significantly larger cross-sectional thoracic areas than previously seen in subjects with healthy lungs (p less than 0.01). No atelectasis was seen in any patient. During anaesthesia there was a further worsening of the VA/Q mismatch with significantly increased log Q SD (1.29, p less than 0.05) but no increase in shunt (mean 1%). Minor atelectatic areas were noted in three patients, the others displayed no atelectasis at all. Chest dimensions were reduced by no more than 3% during anaesthesia, suggesting an unchanged or only minimally affected functional residual capacity. These findings contrast with those seen in patients with healthy lungs in whom atelectasis and shunt regularly develop during anaesthesia.

Aged↗
PubMed1991

Ventilation-perfusion inequality in patients with non-alcoholic liver cirrhosis.

Ventilation-perfusion relationships were studied in patients with non-alcoholic liver cirrhosis. Spirometry was essentially normal but the transfer factor of the lung (DLCO) was reduced by an average 34% of predicted. Arterial oxygen tension (PaO2) ranged from normal down to 6.9 kPa. Varying degrees of ventilation-perfusion (VA/Q) abnormalities (multiple inert gas elimination technique) were observed with increased dispersion of the perfusion distribution (log SDQ, 0.90; range 0.32-1.71; upper normal limit, 0.60) and the presence of both regions of low VA/Q ratios (between 0.1 and 0.005) (mean 4.1%; range 0-18.8%) and shunt (VA/Q ratios below 0.005) (mean 3.9%; range 0.19.8%). There was a close similarity between measured and calculated PaO2 in normoxaemic patients, but calculated values exceeded measured PaO2 in hypoxaemic patients. The difference between calculated and measured PaO2 correlated inversely to DLCO (r = 0.65, p less than 0.05). An inverse correlation was also noted between DLCO and the sum of shunt and low VA/Q regions (r = 0.87, p less than 0.001). It is concluded that hypoxaemia in non-alcoholic liver cirrhosis patients can be accounted for by intrapulmonary shunting and VA/Q mismatch, and possibly a "diffusion-perfusion" defect in patients with more severe gas exchange impairment.

Adult↗
PubMed1990

Decreased lung function and exposure to diisocyanates (HDI and HDI-BT) in car repair painters: observations on re-examination 6 years after initial study.

Thirty-six car painters and 115 control persons participated in a follow-up investigation 6 years after the initial study, including measurement of lung function (dynamic spirometry and nitrogen washout test) and estimation of exposure to diisocyanates based on individual working routines, use of respiratory protection equipment, and measurements. The mean exposure for the car painters was 0.0015 mg/m3 hexamethylenediisocyanate (HDI) and 0.09 mg/m3 hexamethylenediisocyanate-biurettrimer (HDI-BT), but frequently there were peak exposures exceeding 2.0 mg/m3 HDI-BT for at least 30 sec. Compared with smoking controls, the smoking car painters had greater yearly reduction in FVC (95 versus 38 ml), FEV1 (61 versus 28 ml), and VC (77 versus 30 ml). The nonsmoking car painters showed no differences in lung volumes compared with their nonsmoking controls. The impairment correlated well with the frequency of high peak exposures to HDI-BT, but not with the mean exposure to diisocyanates.

Adult↗