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Biomedical subjects

L Gunnarsson

Publications and source records attributed to L Gunnarsson.

8 recordsLinked to original sources

Influence of age on circulation and arterial blood gases in man.

BACKGROUND: Modern data on the influence of age on hemodynamic and blood gas data in healthy subjects are sparse, especially in middle aged or older subjects. Most measurements have been done in patients during major surgery or in intensive care when the patients have one or more failing organ systems. This study reports on hemodynamics, blood gases and blood volume in healthy patients prior to anesthesia and elective surgery. METHODS: A total of 116 subjects (92 males, 24 females) were investigated prior to anesthesia and elective surgery. No one had received any premedication or was taking regular medication. All subjects were in good physical condition, except for their surgical disease, and clinical examination and history did not reveal any sign of cardiopulmonary disease. Measurements were made of systemic and pulmonary vascular pressures, cardiac output, arterial blood gases and blood volume by 131I-Albumin distribution. RESULTS: Cardiac output, stroke volume, and blood volume correlated to body surface. Relating these variables to body size eliminated almost all differences between the male and female groups. These variables, as well as both systemic and pulmonary artery systolic vascular pressures, were affected by increasing age. Pulmonary capillary wedge and right atrial pressures were not influenced by age. PaO2 decreased with age from 14.0 kPa at 20 years to 11.3 kPa at 80, whereas PaCO2 was unaltered. No effect of light smoking was found on pulmonary circulation or arterial blood gases. Significant correlations were found between blood volume on the one hand and body size and age on the other hand, but not in regard to sex.

Adult

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

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

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

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

Anesthesia for liver transplantation in patients with arterial hypoxemia.

Arterial oxygenation during anesthesia and time of postoperative mechanical ventilation were investigated in 17 patients with chronic liver disease who underwent liver transplantation. Six patients had arterial hypoxemia (PaO2 64 +/- 3 mm Hg) and the other 11 patients had normal PaO2 (105 +/- 5 mm Hg) before transplantation. None of the patients were smokers and all had normal preoperative pulmonary X-ray and spirometry. During transplantation, PaO2 increased in both groups, but PaO2 was still approximately 20% lower and PA-aO2 was 40%-60% higher in the hypoxemic group than in the normoxemic patients (P less than 0.05). The median postoperative time on mechanical ventilation was three times longer in the hypoxemic group (56 h) than in the normoxemic patients (18 h; P = NS). Number or severity of postoperative complications and outcome did not differ between the two groups. It is therefore suggested that patients with arterial hypoxemia without overt lung disease should also be accepted for liver transplantation.

Adolescent

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