Biomedical subjects

L Tokics

Publications and source records attributed to L Tokics.

At least 19 recordsLinked to original sources

PubMed1995

Lung function after open versus laparoscopic cholecystectomy.

Postoperative lung function and gas exchange were studied in 36 patients after cholecystectomy. Twenty-four of the patients underwent laparoscopic cholecystectomy while the remaining twelve were operated with open technique. Before surgery all patients had normal ventilatory volumes (forced vital capacity, FVC and forced expired volume in 1 s, FEV1) and normal gas exchange. Two hours postoperatively FVC was reduced to 64 +/- 16% (P < 0.05) of the preoperative level in the laparoscopic group and to 45 +/- 23% (P < 0.05) after open cholecystectomy. On the first postoperative day FVC was virtually normal in the laparoscopic patients (77 +/- 17% of preoperative level, NS), whereas the open surgery patients still had a decreased FVC (56 +/- 13% of preoperative, P < 0.05). FEV1 in the postoperative period followed the same course as FVC. Gas exchange was significantly impaired in the early postoperative period in all patients but no difference between the two groups was found. Two hours postoperatively PaO2 was reduced to 85% (P < 0.05) of preoperative value and PaCO2 had increased by 0.5 kPa (P < 0.05). The alveolo-arterial oxygen tension difference (PA-aO2) had increased by approximately 45% to a mean of 3.7 kPa (P < 0.05). On the first postoperative day gas exchange was still significantly impaired in the open surgery patients. Atelectasis detected by computed X-ray tomography of the lungs were found in both groups. However, the amount of atelectasis tended to be smaller in the laparoscopic group than in the open surgery patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Phrenic nerve stimulation during halothane anesthesia. Effects of atelectasis.

BACKGROUND: Atelectasis formation during anesthesia may be due to loss of respiratory muscle tone, in particular that of the diaphragm. This was tested by tensing the diaphragm by phrenic nerve stimulation (PNS) and observing the effect on atelectasis. METHODS: Twelve patients (mean age 48 yr) without preexisting lung disease were studied during halothane anesthesia. PNS was executed with an external electrode on the right side of the neck. Chest dimensions and area of atelectasis were studied by computed tomography of the chest. RESULTS: Right-sided PNS against an occluded airway at functional residual capacity reduced the atelectatic area in the right lung from 5.1 to 3.8 cm2. The atelectasis was reduced to 1.1 cm2 after application of positive end-expiratory pressure (PEEP) of 10 cmH2O and large tidal volumes but increased to 2.5 cm2 within 1 min after discontinuation of PEEP. Commencement of PNS immediately after PEEP prevented the atelectasis from increasing, the mean area being 0.9 cm2. In seven patients, in whom the trachea was intubated with a double-lumen endobronchial catheter the atelectatic area was smaller during PNS with an open airway than during positive pressure inflation of the lung with the same volume as inspired during PNS (3.5 and 5.2 cm2, respectively. CONCLUSIONS: The findings indicate that contracting the diaphragm in the anesthetized subject reduces the size of atelectasis.

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↗

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

Radiospirometry V/Q.

Single photon emission computerized tomography (SPECT) of the lungs was used for topographical determination of V/Q ratios in anaesthetized-paralyzed subjects. Ventilation and perfusion were estimated from the distribution of an inhaled aerosol containing a radioactive isotope and injected macroaggregates of human albumin tagged with another isotope. There was a prominent gradient of V/Q ratios in the vertical direction. In the horizontal plane there were marked gradients of both ventilation and perfusion of similar appearance with maxima in central lung regions, resulting in only small gradients of V/Q ratios.

Anesthesia, Inhalation↗

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↗

PubMed1990

The influence of body position and differential ventilation on lung dimensions and atelectasis formation in anaesthetized man.

The effects of body position and anaesthesia with mechanical ventilation on thoracic dimensions and atelectasis formation were studied by means of computerized tomography in 14 patients. Induction of anaesthesia in the supine position reduced the cross-sectional area for both lungs and caused atelectasis formation in dependent lung regions in 4/5 patients. Conventional ventilation with positive end-expiratory pressure (PEEP) increased thoracic dimensions and reduced, but did not eliminate, the atelectatic areas. The vertical diameters of both lungs were smaller in the lateral position as compared to the supine position (16.7 vs 10.4 cm in the left lung and 17.3 vs 12.8 cm in the right lung). The lateral positioning also caused a large reduction of the atelectatic area in the non-dependent lung. Differential ventilation with selective PEEP to the dependent lung eliminated (3/8 patients) or reduced (5/8 patients) dependent lung atelectasis. It can be concluded that lung geometry is altered in the lateral position: the shape of the lung makes the vertical diameter of each lung less in the lateral position, compared to the supine position. The atelectatic areas are mainly located in the dependent lung in the lateral position, and these atelectatic areas could be further reduced by selective PEEP to this lung.

Adult↗

PubMed1990

Ventilation-perfusion relationships and atelectasis formation in the supine and lateral positions during conventional mechanical and differential ventilation.

Patients without respiratory symptoms were studied awake and during general anesthesia with mechanical ventilation prior to elective surgery. Ventilation-perfusion (VA/Q) relationships, gas exchange and atelectasis formation were studied during five different conditions: 1) supine, awake; 2) supine during anesthesia with conventional mechanical ventilation (CV); 3) in the left lateral position during CV; 4) as 3) but with 10 cm of positive end-expiratory pressure (PEEP) and 5) as 3) but using differential ventilation with selective PEEP (DV + SPEEP) to the dependent lung. Atelectatic areas and increases of shunt blood flow and blood flow to regions with low VA/Q ratios appeared after induction of anesthesia and CV. With the patients in the lateral position, further VA/Q mismatch with a fall in PaO2 and increased dead space ventilation was observed. Atelectatic lung areas were still present, although the total atelectatic area was slightly decreased. Some of the effects caused by the lateral position could be counteracted by adding PEEP. Perfusion of regions with low VA/Q ratios and venous admixture were then diminished, while PaO2 was slightly increased; shunt blood flow and dead space ventilation were essentially unchanged. During CV + PEEP, there was a decrease in cardiac output, compared to CV in the lateral position. DV + SPEEP was more effective than CV + PEEP in decreasing shunt flow and increasing PaO2 in the lateral position; in addition to this, cardiac output was not affected.

Adult↗

PubMed1990

Atelectasis causes gas exchange impairment in the anaesthetised horse.

The anatomical basis of gas exchange impairment in the anaesthetised horse was studied by computerised tomography (CT; three shetland ponies) and morphological analysis (one pony and three horses). By means of CT, densities were seen in dependent lung regions early during anaesthesia, both with spontaneous breathing and with mechanical ventilation. The densities remained for some time where they had initially been created when the animal was turned from dorsal to sternal recumbency. Deep insufflation of the lungs reduced the dense area. Gas exchange was impaired roughly in proportion to the dense area. On histological analysis, the densities were atelectatic and congested with blood. Gravimetry showed no more extravascular water per unit lung tissue in the atelectatic than in the 'normal' regions, and the blood content was increased only slightly. It is concluded that the horse develops atelectasis in dependent lung regions early during anaesthesia in dorsal recumbency, and that atelectasis is the most likely explanation for the large shunt and impaired arterial oxygenation regularly seen during anaesthesia.

Anesthesia↗

PubMed1989

Atelectasis and gas exchange impairment during enflurane/nitrous oxide anaesthesia.

The development of atelectasis and effects on gas exchange during enflurane anaesthesia in nitrogen/oxygen or nitrous oxide/oxygen (inspired oxygen fraction 0.4) were studied in 16 lung-healthy patients (mean age 49 years). Awake, no subject displayed atelectasis as assessed by computed x-ray tomography of the thorax. Pulmonary gas exchange, studied by multiple inert gas elimination technique, and blood gases were normal. After 10 min of enflurane anaesthesia in nitrogen/oxygen, 14 of 16 subjects had developed atelectasis. After 30 min of enflurane anaesthesia in nitrogen/oxygen or nitrous oxide/oxygen, all patients had developed atelectasis, and a further increase was observed after 90 min of anaesthesia to approximately 5% of the intrathoracic area. There was no difference between the two anaesthesia groups. In the nitrogen group, shunt rose to a maximum of 5.8% at 30 min of enflurane anaesthesia, with a significant reduction to the initial anaesthesia level after 90 min of anaesthesia (3.4%). Perfusion of poorly ventilated lung regions (low VA/Q) averaged 4-5% and did not vary significantly during the anaesthesia. In the nitrous oxide group, shunt increased to 6.3% after 90 min of anaesthesia, and there was a parallel decrease in perfusion of low VA/Q regions. The findings suggest that besides prompt collapse of lung tissue during induction of anaesthesia, absorption of gas from closed-off or poorly ventilated regions takes place and further increases the atelectatic area.

Adult↗

PubMed1989

Pulmonary densities during anaesthesia. An experimental study on lung morphology and gas exchange.

The nature of dense areas in dependent lung regions regularly seen in anaesthetized humans was examined in a sheep model. During anaesthesia with muscle paralysis and mechanical ventilation dense areas in dependent lung regions could be seen by means of computerized tomography (CT). They had the same location and the same attenuation as in anaesthetized humans. Gas exchange impairment tended to increase in proportion to the size of the dense area on the CT scan. Microscopy showed that the densities in the sheep were atelectatic lung regions, with no or little interstitial oedema and only minor vascular congestion. The atelectatic lung tissue was sharply demarcated and the lung tissue in the immediate vicinity was well aerated, or even hyperinflated. Gravimetry showed the same amount of extravascular fluid and blood per unit lung weight in the atelectatic lung and in the aerated lung region. It is concluded that the densities appearing in dependent lung regions during anaesthesia are caused by atelectasis.

Anesthesia↗

PubMed1988

Thoracoabdominal restriction in supine men: CT and lung function measurements.

Thoracoabdominal restriction was brought on by means of a corset, and the subsequent effects on thoracic dimensions and lung tissue were studied by computerized tomography (CT) and by various lung function tests in supine healthy volunteers (mean age 30 yr). Restriction caused reductions in total lung capacity (helium equilibration) from mean 6.84 to 4.80 liters, in functional residual capacity (FRC) from 2.65 to 2.08 liters, and in vital capacity from 5.16 to 3.45 liters. Closing capacity (single-breath N2 washout) fell from 2.42 to 1.88 liters, thus matching the reduction in FRC. The static pressure-lung volume curve was shifted to the right by 1.5 cmH2O at 50% of total lung capacity. However, no change in the slope of the curve was observed. The diaphragm was moved cranially by 1.2 cm, and the thoracic cross-sectional area was reduced by a mean 32 cm2 at a level just above the diaphragm. No changes in the lung tissue were seen on CT scanning. Gas exchange, as assessed by multiple inert gas elimination technique and arterial blood gas analysis, was unaffected by restriction. It is concluded that in supine subjects, thoracoabdominal restriction that reduces FRC by 0.6 liter is not accompanied by atelectasis (normal CT scan). In this respect the result differs from that found in anesthetized supine subjects who show the same fall in FRC and atelectasis in dependent lung regions.

Abdomen↗

PubMed1987

Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure.

Lung densities (atelectasis) and pulmonary gas exchange were studied in 13 supine patients with no apparent lung disease, the former by transverse computerized tomography (CT) and the latter by a multiple inert gas elimination technique for assessment of the distribution of ventilation/perfusion ratios. In the awake state no patient had clear signs of atelectasis on the CT scan. Lung ventilation and perfusion were well matched in most of the patients. Three patients had shunts corresponding to 2-5% of cardiac output, and in one patient there was low perfusion of poorly ventilated regions. CT scans after 15 min of halothane anesthesia and mechanical ventilation showed densities in dependent lung regions in 11 patients. A shunt was present in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. Ventilation of poorly perfused regions was noted in nine patients, ranging from 1-19% of total ventilation. The magnitude of the shunt significantly correlated to the size of dependent densities (r = 0.84, P less than 0.001). Five patients studied during spontaneous breathing under anesthesia displayed both densities in dependent regions and a shunt, although of fairly small magnitude (1.8% and 3.7%, respectively). Both the density area and the shunt increased after muscle paralysis. PEEP reduced the density area in all patients but did not consistently alter the shunt. It is concluded that the development of atelectasis in dependent lung regions is a major cause of gas exchange impairment during halothane anesthesia, during both spontaneous breathing and mechanical ventilation, and that PEEP diminishes the atelectasis, but not necessarily the shunt.

Adult↗

PubMed1987

Constitutional factors promoting development of atelectasis during anaesthesia.

The extent of atelectasis was correlated to constitutional factors in 38 patients who underwent computed tomography prior to and during general anaesthesia with halothane. All patients but two developed atelectasis in dependent regions of both lungs immediately after induction of anaesthesia prior to surgery. The transverse area of the densities ranged from 0 to 27 cm2, and there were no significant differences between patients of different age or sex, or with different smoking habits. A significant linear regression was found between Broca's index weight (kg)/height (cm)-100 and the area of the densities, and also between an index describing the shape of the thorax and the density area. Thus, patients who were overweight and/or had a low and wide thorax tended to develop more extensive atelectasis during anaesthesia. This finding might partly explain why overweight patients develop postoperative pulmonary complications more often than non-obese patients.

Adult↗

PubMed1987

Postoperative analgesia with intrapleural administration of bupivacaine-adrenaline.

Twenty-one patients who underwent elective cholecystectomy were studied with regard to the effect of intrapleural administration of bupivacaine-adrenaline solution on postoperative pain and ventilatory capacity. Administration of 10 or 20 ml of 2.5 mg/ml or 5 mg/ml bupivacaine solution resulted in complete analgesia in 143 of 159 administrations. Most patients experienced the maximal pain-relieving effect within 1-2 min and analgesia persisted as a rule for 3-5 h. Forced vital capacity and forced expiratory volume in 1 s increased after intrapleural analgesia on average by 56% and 46%, respectively, on the first postoperative day and by 35% and 51%, respectively, on the second day. There was no significant difference in the analgesic effect or in the effect on the ventilatory capacity between the 2.5 mg/ml or the 5 mg/ml solution, in either the 10 ml or the 20 ml dose. Placebo (NaCl) given intrapleurally had no effect on pain or on the ventilatory capacity. The plasma concentration of bupivacaine after intrapleural administration showed a wide interindividual variation, with considerably higher average values when the 5 mg/ml solution had been used than for the 2.5 mg/ml solution. Although no toxic effects were noted, a 2.5 mg/ml solution, which can be given in an initial dose of 20 ml and top-up doses of 10 ml at 3-6 h intervals, is recommended. In four patients minor pneumothorax developed when the catheter was introduced. The pneumothorax was easily evacuated, but underlines the need for great care when introducing the catheter.

Adult↗

PubMed1987

Computerized tomography of the chest and gas exchange measurements during ketamine anaesthesia.

The effects of atelectasis on pulmonary gas exchange were studied in eight supine, clinically lung-healthy patients. Atelectasis was studied by computerized tomography (CT), and gas exchange by blood gas analysis. The distribution of ventilation/perfusion ratios was assessed by a multiple inert gas elimination technique. No patient had any signs of atelectasis in the awake state, and gas exchange was normal. During ketamine anaesthesia and spontaneous breathing, lung ventilation and perfusion were well matched in most subjects. In one patient there was perfusion of poorly ventilated regions amounting to 14% of cardiac output, and in another there was a shunt of 4% of cardiac output; this patient was the only one who developed atelectasis in dependent lung regions. After muscular relaxation and commencement of mechanical ventilation, all patients but one developed both shunt (2-6% of cardiac output) and atelectasis. The shunt correlated to the size of atelectasis. It is concluded that the occurrence of shunt during anaesthesia is related to the development of atelectasis in dependent lung region, which is consistent with the hypothesis that it is changes in chest-wall mechanics that cause atelectasis.

Adult↗

PubMed1986

Atelectasis during anaesthesia and in the postoperative period.

Transverse sections of lung tissue were studied in patients by computerized tomography during anaesthesia and in the postoperative period. Eight patients were studied during intravenous (thiopentone) and six during inhalational (halothane) anaesthesia. The latter patients were studied during both spontaneous and mechanical ventilation. Five of the patients who underwent surgery for inguinal hernia and five patients in whom laparotomy was performed were studied 1 h and 24 h postoperatively. No patient showed any lung changes while awake preoperatively, and all patients developed dependent, crest-shaped lung densities within 5-10 min of anaesthesia. The densities comprised 3.4% of the lung volume in the caudal (basal) 5 cm of the lung tissue. No significant differences in the size and distribution of the densities were noted between spontaneous breathing and mechanical ventilation during anaesthesia, or between intravenous and inhalational anaesthesia. The densities remained in nine of ten patients 1 h postoperatively, and they remained in five of ten patients 24 h after anaesthesia. The densities are considered to be compression atelectases which may develop as a result of relaxation of the diaphragm. They may be important contributors to postoperative pulmonary complications.

Adult↗

PubMed1986

Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis.

Pulmonary gas exchange and the development of atelectasis were studied in eight essentially lung-healthy patients, awake and during halothane anaesthesia with mechanical ventilation. Gas exchange was evaluated by a multiple inert-gas elimination technique and conventional blood-gas analysis, and atelectasis was studied by computerized tomography (CT). Ventilation and lung perfusion were well matched in the majority of the patients when awake. In two patients there was low perfusion of poorly ventilated regions (low VA/Q). One patient had a shunt corresponding to 4% of cardiac output. None of the patients showed signs of atelectasis on the CT scans. After 15 min of anaesthesia, shunt had appeared in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. The major VA/Q mode was widened and ventilation of poorly perfused regions (high VA/Q) was noted in seven patients. Densities in dependent lung regions (interpreted as atelectasis) were seen on the CT scans in six patients. The extent of atelectasis was significantly correlated both to the magnitude of shunt (r = 0.93, P less than 0.01) and to the impairment of arterial oxygenation (r = 0.99, P less than 0.001). The findings indicate that atelectasis in dependent lung regions during halothane anaesthesia creates shunting of blood flow and that atelectasis is the major or sole cause of impaired gas exchange in the lung-healthy, anaesthetized subject.

Adult↗