Biomedical subjects

L Tokics

Publications and source records attributed to L Tokics.

33 records · Page 2Linked to original sources

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↗

PubMed1986

Densities in dependent lung regions during anaesthesia: atelectasis or fluid accumulation?

In previous studied with computed tomography (CT) prior to and during general anaesthesia, we found that densities developed in dependent parts of the lungs immediately after induction of anaesthesia in all examined patients. It was suggested that the densities were atelectases created by compression of lung tissue but an alternative explanation could be accumulation of extravascular fluid in the lung tissue and/or in the pleural space. In the present study the nature of the densities was analysed in further detail. Injections of contrast medium into the pleural space revealed that the densities were located in the lung tissue and not in the pleural space. By injecting contrast medium intravenously and repeating the CT scanning over a 2-min period the passage of contrast through the major vessels and the lung densities could be studied. The transit time of the contrast medium was of the same magnitude in the densities and the major lung vessels. This indicates that there were no regions with an increased amount of extravascular fluid to delay the contrast passage. These findings oppose the idea of fluid accumulation as the cause of the densities, while atelectasis remains the most plausible explanation.

Adult↗

PubMed1986

Splanchnic blood flow during halothane-relaxant anaesthesia in elderly patients.

We have previously found that halothane-relaxant anaesthesia in elderly patients causes a change towards a hyperkinetic circulation, with a decrease in the arterial-mixed venous oxygen content difference. This could be attributed to vasodilation. In the present study the splanchnic contribution to these changes was investigated. Nine patients were studied during halothane-relaxant anaesthesia prior to surgery. During anaesthesia splanchnic blood flow was markedly reduced, while splanchnic oxygen uptake decreased only moderately compared with the awake level. This resulted in an increase in splanchnic oxygen extraction. It is concluded that the splanchnic vascular bed does not contribute to the "hyperkinetic" circulation during halothane anaesthesia.

Aged↗

PubMed1985

Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation.

Functional residual capacity (FRC), rib cage and abdominal dimensions (rc-ab), central blood volume (CBV), and extra vascular lung water (EVLW) were measured in six lung-healthy subjects awake and during halothane anesthesia, muscle paralysis, and mechanical ventilation. FRC was assessed by multiple breath nitrogen washout, rc-ab dimensions by computerized tomography, and CBV and EVLW by a double-indicator dilution technique (thermo-dye). During anesthesia, FRC decreased by 0.5 1 (17%). The cross-sectional chest area was reduced by 12-20 cm2, causing an approximate reduction in thoracic volume by 0.3 1. Concomitantly, the diaphragm was moved cranially by an average of 1.9 cm, diminishing the thoracic volume a further 0.5 1. The abdominal cross-sectional area did not alter significantly, despite the shift of the diaphragm. CBV decreased by 0.3 1. EVLW did not change significantly. It is concluded that the thoracic volume is reduced during halothane anesthesia, muscle paralysis, and mechanical ventilation as a result of cranial shift of the diaphragm and reduction in transverse area. The decrease in thoracic volume is accompanied by a reduction in FRC and a displacement of blood from the thorax to the abdomen, the transverse area of the latter thus being maintained despite the shift of the diaphragm.

Abdomen↗

PubMed1985

Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis.

Twenty patients (23-76 yr) were studied with regard to lung tissue changes prior to and following induction of general anesthesia with muscular relaxation, and another four subjects were studied for a longer period awake. The transverse thoracic area and the structure of the lung tissue were determined by computerized tomography. No abnormalities in the lung tissue were noted before anesthesia. Within 5 min after induction, including muscular relaxation, all subjects had developed crest-shaped changes of increased density in the dependent regions of both lungs. They were largest in the most caudal segment (4.8 +/- 0.8% of the transverse lung area, mean +/- SE) and smaller in the cephalad exposures (3.4 +/- 0.7% of the transverse area). The size of the densities showed no correlation to age. The densities did not increase after a further 20 min of anesthesia and were not affected by the inspiratory oxygen fraction. When the subjects were moved from the supine to the lateral position, the crest-shaped densities disappeared in the nondependent lung and remained in the dorsal part of the dependent lung. The application of positive end-expiratory pressure of 10 cmH2O eliminated or reduced the densities. The four awake subjects showed no lung densities after 90 min in the supine position. It is suggested that these crest-shaped densities represent atelectases, which develop by compression of lung tissue rather than by resorption of gas.

Adult↗

PubMed1985

Halothane-relaxant anaesthesia in elderly patients.

Twenty-three elderly patients, scheduled for elective cholecystectomy, were studied during halothane-relaxant anaesthesia. Anaesthesia was induced with thiopentone and maintained with halothane in 12 patients, six of whom had also received premedication. Eleven patients were anaesthetized with halothane, without thiopentone induction and with no premedication. Measurements of central haemodynamics were performed awake and during anaesthesia at end-tidal halothane concentrations of 0.5 and 1.0%; at the lower concentration, measurements were also made after addition of nitrous oxide. Premedication and thiopentone had no influence on the subsequent halothane anaesthesia. Halothane caused reductions of cardiac index, mean arterial blood pressure and oxygen uptake. However, neither right atrial nor pulmonary capillary venous pressure increased and the arterio-venous oxygen content difference decreased. These findings differ from those made by others in younger subjects and are probably attributable to a dose-dependent reduction in systemic vascular resistance. The addition of nitrous oxide had only minor effects on central circulation. The results suggest that the age of the patients influences their reaction to halothane anaesthesia.

Aged↗

PubMed1985

New aspects on atelectasis during anaesthesia.

Sixteen subjects were studied with regard to lung tissue changes during general anaesthesia. The transverse area and the structure of the lung tissue were studied by computerized tomography. No abnormalities were noted in the lung tissue before anaesthesia, but within five minutes after induction, all subjects had developed crest-shaped dependent changes of an increased density in both lungs. They correspond to 4 - 5 per cent of the total transverse area. The size of the densities could not be correlated to the age of the subjects, or time of the anaesthesia, and they were not affected by the inspiratory oxygen fraction. They could be rotated by turning the patient, and the application of a positive end-expiratory pressure eliminated or reduced the densities. It is suggested that the densities are atelectases, which develop by compression of lung tissue, and not by gas resorption.

Aging↗

PubMed1985

What causes the lowered FRC during anaesthesia?

Functional residual capacity (FRC) by means of body plethysmography chest-abdomen dimensions by whole body computerized tomography, central blood volume (CBV) by double-indicator dilution technique and extremity (peripheral) blood volume (PBV) by segmental thigh and upper arm plethysmography, were assessed in lung-healthy patients who were to undergo general anaesthesia and elective surgery. Anaesthesia was induced by thiopentone and was maintained either by a continuous drip of thiopentone or by inhalation of halothane. Muscle relaxation was obtained by pancuronium bromide. Anaesthesia caused a reduction of the total thoracic volume by an average of 0.75 1. This followed from a cranial shift of the diaphragm and to less extent by a reduced transversal chest area. FRC was concomitantly reduced by an average of 0.5 1 and the CBV, mainly thoracic blood, was reduced by 0.25 - 0.3 1. PBV was slightly reduced by 0.1 1, and it is concluded that these fractions of CBV and TBV must have been pooled in the abdomen. This pooling resulted in more or less maintained transversal abdomen area despite the cranial shift of the diaphragm.

Anesthesia, General↗

PubMed1983

Oxygen uptake and central circulation during ketamine anaesthesia.

Cardiac output, oxygen uptake and plasma catecholamines were studied in patients when awake and during ketamine anaesthesia prior to and during upper abdominal surgery. Oxygen uptake was determined by using a masspectrometer and cardiac output was measured according to the Fick principle. Plasma catecholamines were analysed by high performance liquid chromatography. Stroke volume had fallen by 27% while heart rate had increased after 15 min of anaesthesia, maintaining cardiac output at the awake level. Concomitantly, the oxygen uptake had fallen by 18%. During the succeeding hour of anaesthesia and surgery, cardiac output displayed a transient decrease and oxygen uptake returned to the awake value. The plasma adrenaline concentration fell during the initial phase of anaesthesia and then returned to the awake level. The noradrenaline concentration was increased during the whole anesthetic period. The data suggest a relationship between oxygen uptake and cardiac output during ketamine anaesthesia, similar to that seen during neurolept-nitrous oxide and halothane anaesthesia, except for the initial hyperkinetic period following the induction. No relationship could be shown between catecholamine concentrations in plasma and the central haemodynamics.

Abdomen↗

PubMed1982

Oxygen uptake, plasma catecholamines and cardiac output during neurolept-nitrous oxide and halothane anaesthesias.

Cardiac output, oxygen uptake and plasma catecholamines were studied in patients both awake and during anaesthesia prior to and during upper abdominal surgery. Two different forms of anaesthesia were used: neurolept-nitrous oxide (NLA) and halothane (HALO) anaesthesia. Oxygen uptake was determined by using a masspectrometer, and cardiac output was measured according to the Fick principle. Plasma catecholamines were analysed by high performance liquid chromatography. Cardiac output fell by 40% during NLA and by 30% during HALO. Concomitantly, the oxygen uptake fell by 40% and 35%, respectively. A linear relationship between cardiac output and oxygen uptake could be established both in the awake state and during anaesthesia, with no significant change in the slope or position of the regression line when anaesthesia was commenced. Ventricular filling pressures fell during both anaesthetic procedures. Adrenaline fell to half the plasma concentrations seen in normal subjects under resting conditions, while noradrenaline returned to normal from an initially 30-40% increased value. Surgery caused no significant changes in either cardiac output or oxygen uptake, whereas plasma adrenaline increased by 20 times and noradrenaline by 60-90%. The findings suggest that the reduced oxygen uptake during anaesthesia causes the fall in cardiac output rather than any cardiodepressant action of the anaesthetic. It is possible that the anaesthetic depresses whole-body metabolism by either blocking the effects of catecholamines or interfering with cellular metabolism.

Aged↗