Pulmonary Atelectasis
Coagulation Protein Disorders
Airway closure, atelectasis and gas exchange during general anaesthesia. (1/295)
Airway closure and the formation of atelectasis have been proposed as important contributors to impairment of gas exchange during general anaesthesia. We have elucidated the relationships between each of these two mechanisms and gas exchange. We studied 35 adults with healthy lungs, undergoing elective surgery. Airway closure was measured using the foreign gas bolus technique, atelectasis was estimated by analysis of computed x-ray tomography, and ventilation-perfusion distribution (VA/Q) was assessed by the multiple inert gas elimination technique. The difference between closing volume and expiratory reserve volume (CV-ERV) increased from the awake to the anaesthetized state. Linear correlations were found between atelectasis and shunt (r = 0.68, P < 0.001), and between CV-ERV and the amount of perfusion to poorly ventilated lung units ("low Va/Q", r = 0.57, P = 0.001). Taken together, the amount of atelectasis and airway closure may explain 75% of the deterioration in PaO2. There was no significant correlation between CV-ERV and atelectasis. We conclude that in anaesthetized adults with healthy lungs, undergoing mechanical ventilation, both airway closure and atelectasis contributed to impairment of gas exchange. Atelectasis and airway closure do not seem to be closely related. (+info)Kinetics of absorption atelectasis during anesthesia: a mathematical model. (2/295)
Recent computed tomography studies show that inspired gas composition affects the development of anesthesia-related atelectasis. This suggests that gas absorption plays an important role in the genesis of the atelectasis. A mathematical model was developed that combined models of gas exchange from an ideal lung compartment, peripheral gas exchange, and gas uptake from a closed collapsible cavity. It was assumed that, initially, the lung functioned as an ideal lung compartment but that, with induction of anesthesia, the airways to dependent areas of lung closed and these areas of lung behaved as a closed collapsible cavity. The main parameter of interest was the time the unventilated area of lung took to collapse; the effects of preoxygenation and of different inspired gas mixtures during anesthesia were examined. Preoxygenation increased the rate of gas uptake from the unventilated area of lung and was the most important determinant of the time to collapse. Increasing the inspired O2 fraction during anesthesia reduced the time to collapse. Which inert gas (N2 or N2O) was breathed during anesthesia had minimal effect on the time to collapse. (+info)'Alveolar recruitment strategy' improves arterial oxygenation during general anaesthesia. (3/295)
Abnormalities in gas exchange during general anaesthesia are caused partly by atelectasis. Inspiratory pressures of approximately 40 cm H2O are required to fully re-expand healthy but collapsed alveoli. However, without PEEP these re-expanded alveoli tend to collapse again. We hypothesized that an initial increase in pressure would open collapsed alveoli; if this inspiratory recruitment is combined with sufficient end-expiratory pressure, alveoli will remain open during general anaesthesia. We tested the effect of an 'alveolar recruitment strategy' on arterial oxygenation and lung mechanics in a prospective, controlled study of 30 ASA II or III patients aged more than 60 yr allocated to one of three groups. Group ZEEP received no PEEP. The second group received an initial control period without PEEP, and then PEEP 5 cm H2O was applied. The third group received an increase in PEEP and tidal volumes until a PEEP of 15 cm H2O and a tidal volume of 18 ml kg-1 or a peak inspiratory pressure of 40 cm H2O was reached. PEEP 5 cm H2O was then maintained. There was a significant increase in median PaO2 values obtained at baseline (20.4 kPa) and those obtained after the recruitment manoeuvre (24.4 kPa) at 40 min. This latter value was also significantly higher than PaO2 measured in the PEEP (16.2 kPa) and ZEEP (18.7 kPa) groups. Application of PEEP also had a significant effect on oxygenation; no such intra-group difference was observed in the ZEEP group. No complications occurred. We conclude that during general anaesthesia, the alveolar recruitment strategy was an efficient way to improve arterial oxygenation. (+info)Dynamics of re-expansion of atelectasis during general anaesthesia. (4/295)
A major cause of impaired gas exchange during general anaesthesia is atelectasis, causing pulmonary shunt. A 'vital capacity' (VC) manoeuvre (i.e. inflation of the lungs up to 40 cm H2O, maintained for 15 s) may re-expand atelectasis and improve oxygenation. However, such a manoeuvre may cause adverse cardiovascular effects. Reducing the time of maximal inflation may improve the margin of safety. The aim of this study was to analyse the change over time in the amount of atelectasis during a VC manoeuvre in 12 anaesthetized adults with healthy lungs. I.v. anaesthesia with controlled mechanical ventilation (VT 9 (SD 1) ml kg-1) was used. For the VC manoeuvre, the lungs were inflated up to an airway pressure (Paw) of 40 cm H2O. This pressure was maintained for 26 s. Atelectasis was assessed by analysis of computed x-ray tomography. The amount of atelectasis, measured at the base of the lungs, was 4.0 (SD 2.7) cm2 after induction of anaesthesia. The decrease in the amount of atelectasis over time during the VC manoeuvre was described by a negative exponential function with a time constant of 2.6 s. At an inspired oxygen concentration of 40%, PaO2 increased from 17.2 (4.0) kPa before to 22.2 (6.0) kPa (P = 0.013) after the VC manoeuvre. Thus in anaesthetized adults undergoing mechanical ventilation with healthy lungs, inflation of the lungs to a Paw of 40 cm H2O, maintained for 7-8 s only, may re-expand all previously collapsed lung tissue, as detected by lung computed tomography, and improve oxygenation. We conclude that the previously proposed time for a VC manoeuvre may be halved in such subjects. (+info)Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection. (5/295)
BACKGROUND: High concentrations of inspired oxygen are associated with pulmonary atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. The authors tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% perioperative oxygen. METHODS: Thirty patients aged 18-65 yr were anesthetized with isoflurane and randomly assigned to 30% or 80% oxygen during and for 2 h after colon resection. Chest radiographs and pulmonary function tests (forced vital capacity and forced expiratory volume) were obtained preoperatively and on the first postoperative day. Arterial blood gas measurements were obtained intraoperatively, after 2 h of recovery, and on the first postoperative day. Computed tomography scans of the chest were also obtained on the first postoperative day. RESULTS: Postoperative pulmonary mechanical function was significantly reduced compared with preoperative values, but there was no difference between the groups at either time. Arterial gas partial pressures and the alveolar-arterial oxygen difference were also comparable in the two groups. All preoperative chest radiographs were normal. Postoperative radiographs showed atelectasis in 36% of the patients in the 30%-oxygen group and in 44% of those in the 80%-oxygen group. Relatively small amounts of pulmonary atelectasis (expressed as a percentage of total lung volume) were observed on the computed tomography scans, and the percentages (mean +/- SD) did not differ significantly in the patients given 30% oxygen (2.5% +/- 3.2%) or 80% oxygen (3.0% +/- 1.8%). These data provided a 99% chance of detecting a 2% difference in atelectasis volume at an alpha level of 0.05. CONCLUSIONS: Lung volumes, the incidence and severity of atelectasis, and alveolar gas exchange were comparable in patients given 30% and 80% perioperative oxygen. The authors conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis. (+info)Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. (6/295)
BACKGROUND: Morbidly obese patients, during anesthesia and paralysis, experience more severe impairment of respiratory mechanics and gas exchange than normal subjects. The authors hypothesized that positive end-expiratory pressure (PEEP) induces different responses in normal subjects (n = 9; body mass index < 25 kg/m2) versus obese patients (n = 9; body mass index > 40 kg/m2). METHODS: The authors measured lung volumes (helium technique), the elastances of the respiratory system, lung, and chest wall, the pressure-volume curves (occlusion technique and esophageal balloon), and the intraabdominal pressure (intrabladder catheter) at PEEP 0 and 10 cm H2O in paralyzed, anesthetized postoperative patients in the intensive care unit or operating room after abdominal surgery. RESULTS: At PEEP 0 cm H2O, obese patients had lower lung volume (0.59 +/- 0.17 vs. 2.15 +/- 0.58 l [mean +/- SD], P < 0.01); higher elastances of the respiratory system (26.8 +/- 4.2 vs. 16.4 +/- 3.6 cm H2O/l, P < 0.01), lung (17.4 +/- 4.5 vs. 10.3 +/- 3.2 cm H2O/l, P < 0.01), and chest wall (9.4 +/- 3.0 vs. 6.1 +/- 1.4 cm H2O/l, P < 0.01); and higher intraabdominal pressure (18.8 +/-7.8 vs. 9.0 +/- 2.4 cm H2O, P < 0.01) than normal subjects. The arterial oxygen tension was significantly lower (110 +/- 30 vs. 218 +/- 47 mmHg, P < 0.01; inspired oxygen fraction = 50%), and the arterial carbon dioxide tension significantly higher (37.8 +/- 6.8 vs. 28.4 +/- 3.1, P < 0.01) in obese patients compared with normal subjects. Increasing PEEP to 10 cm H2O significantly reduced elastances of the respiratory system, lung, and chest wall in obese patients but not in normal subjects. The pressure-volume curves were shifted upward and to the left in obese patients but were unchanged in normal subjects. The oxygenation increased with PEEP in obese patients (from 110 +/-30 to 130 +/- 28 mmHg, P < 0.01) but was unchanged in normal subjects. The oxygenation changes were significantly correlated with alveolar recruitment (r = 0.81, P < 0.01). CONCLUSIONS: During anesthesia and paralysis, PEEP improves respiratory function in morbidly obese patients but not in normal subjects. (+info)Reverse mismatched ventilation-perfusion pulmonary imaging with accumulation of technetium-99m-DTPA in a mucous plug in a main bronchus: a case report. (7/295)
The phenomenon of reverse mismatched ventilation-perfusion on pulmonary scintigraphy is a fairly common occurrence. We present a patient who was experiencing decreasing oxygen saturation and had a reverse mismatched ventilation-perfusion imaging pattern associated with radiotracer retention in a main bronchus. Technetium-99m-DTPA aerosol lung imaging showed tracer retention in the trachea and right main bronchus, absent ventilation in the right lung, and normal ventilation in the left lung. Technetium-99m-MAA perfusion lung images showed normal perfusion of the left lung and some perfusion in the right lung. These findings represented a reverse ventilation-perfusion mismatch. Reverse mismatched ventilation-perfusion, or totally absent ventilation with preservation of some perfusion in the right lung, resulted in functional intrapulmonary shunting, which explained the decreasing oxygen saturation observed in this patient. A concurrent portable chest radiograph showed elevation of the right hemidiaphragm, a shift of the mediastinum to the right, deviation of the endotracheal tube, narrowing of the intercostal space of the right thorax, and collapse of the right lower lobe. The radiographic findings of underventilation of the right lung with atelectasis of the right lower lobe were due to mucous plugging the right main bronchus. (+info)Targeted disruption of NDST-1 gene leads to pulmonary hypoplasia and neonatal respiratory distress in mice. (8/295)
In order to address the biological function of GlcNAc N-deacetylase/N-sulfotransferase-1 (NDST-1), we disrupted the NDST-1 gene by homologous recombination in mouse embryonic stem cells. The NDST-1 null mice developed respiratory distress and atelectasis that subsequently caused neonatal death. Morphological examination revealed type II pneumocyte immaturity, which was characterized by an increased glycogen content and a reduced number of lamellar bodies and microvilli. Biochemical analysis further indicated that both total phospholipids and disaturated phosphatidylcholine were reduced in the mutant lung. Our data revealed that NDST-1 was essential for the maturation of type II pneumocytes and its inactivation led to a neonatal respiratory distress syndrome. (+info)Pulmonary atelectasis is a medical condition characterized by the collapse or closure of the alveoli (tiny air sacs) in the lungs, leading to reduced or absent gas exchange in the affected area. This results in decreased lung volume and can cause hypoxemia (low oxygen levels in the blood). Atelectasis can be caused by various factors such as obstruction of the airways, surfactant deficiency, pneumothorax, or compression from outside the lung. It can also occur after surgical procedures, particularly when the patient is lying in one position for a long time. Symptoms may include shortness of breath, cough, and chest discomfort, but sometimes it may not cause any symptoms, especially if only a small area of the lung is affected. Treatment depends on the underlying cause and may include bronchodilators, chest physiotherapy, or even surgery in severe cases.
Coagulation protein disorders are a group of medical conditions that affect the body's ability to form blood clots properly. These disorders can be caused by genetic defects or acquired factors, such as liver disease or vitamin K deficiency.
The coagulation system is a complex process that involves various proteins called clotting factors. When there is an injury to a blood vessel, these clotting factors work together in a specific order to form a clot and prevent excessive bleeding. In coagulation protein disorders, one or more of these clotting factors are missing or not functioning properly, leading to abnormal bleeding or clotting.
There are several types of coagulation protein disorders, including:
1. Hemophilia: This is a genetic disorder that affects the clotting factor VIII or IX. People with hemophilia may experience prolonged bleeding after injuries, surgery, or dental work.
2. Von Willebrand disease: This is another genetic disorder that affects the von Willebrand factor, a protein that helps platelets stick together and form a clot. People with this condition may have nosebleeds, easy bruising, and excessive bleeding during menstruation or after surgery.
3. Factor XI deficiency: This is a rare genetic disorder that affects the clotting factor XI. People with this condition may experience prolonged bleeding after surgery or trauma.
4. Factor VII deficiency: This is a rare genetic disorder that affects the clotting factor VII. People with this condition may have nosebleeds, easy bruising, and excessive bleeding during menstruation or after surgery.
5. Acquired coagulation protein disorders: These are conditions that develop due to other medical factors, such as liver disease, vitamin K deficiency, or the use of certain medications. These disorders can affect one or more clotting factors and may cause abnormal bleeding or clotting.
Treatment for coagulation protein disorders depends on the specific condition and severity of symptoms. In some cases, replacement therapy with the missing clotting factor may be necessary to prevent excessive bleeding. Other treatments may include medications to control bleeding, such as desmopressin or antifibrinolytic agents, and lifestyle changes to reduce the risk of injury and bleeding.
A lung is a pair of spongy, elastic organs in the chest that work together to enable breathing. They are responsible for taking in oxygen and expelling carbon dioxide through the process of respiration. The left lung has two lobes, while the right lung has three lobes. The lungs are protected by the ribcage and are covered by a double-layered membrane called the pleura. The trachea divides into two bronchi, which further divide into smaller bronchioles, leading to millions of tiny air sacs called alveoli, where the exchange of gases occurs.