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Query: HUMANGGP:003739 (CO2)
 48,959 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During hysteroscopy the uterus may be distended with carbon dioxide (CO2), nitrous oxide (N2O), or Hyskon (a high molecular weight dextran). An initial study in 27 patients (group 1) using arterialized venous blood samples demonstrated rises in carbon dioxide tension (PCO2) when N2O was insufflated by using a laparoscopy insufflating device--a constant-pressure, variable-volume gas source. Cardiovascular collapse occurred in one patient in this group, most probably as a result of macropulmonary emboli of N2O. The rise in PCO2 is accounted for by an increase in physiologic dead space. In another 24 patients (group 2) the gaseous media were introduced by using a constant-volume, variable-pressure gas source; this resulted in minimal changes in arterial PCO2. The choice of whether a gaseous or liquid distending medium is used for hysteroscopy is governed by the state of the endometrium. If a gaseous medium is indicated, then CO2 is preferable to N2O and should be introduced with a constant-volume, variable-pressure gas source.
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PMID:Blood carbon dioxide tension changes during hysteroscopy. 46

Cardiorespiratory reactions to tilt tests were compared in 80 healthy male subjects with an adequate orthostatic tolerance and in 19 subjects who fainted during tilting. They showed significant differences in the gas exchange, hemodynamics, and external respiration. Variations in the heart rate, pulmonary ventilation and the alveolar CO2 tension were most demonstrative. The findings, particularly the lack of the expected decrease o= oxygen consumption in the presyncopal state contribute to the concepts of the pathogenesis of the orthostatic collapse.
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PMID:[External respiration and gas metabolism in orthostatic syncopes]. 65 94

This article has reviewed the anatomic, compliance, reflex, and respiratory muscle variables that affect upper airway caliber and abnormalities which may precipitate upper airway collapse during sleep. One or more of these variables may be important in the mechanism of OSA in any given patient. First, anyone with anatomic narrowing of the upper airway is susceptible to OSA. However, we do know if anatomic narrowing of the upper airway is necessary for the development of OSA. Surely, heavy snoring produces pharyngeal trauma and possibly edema or inflammation, which in turn may narrow the upper airway. Submucosal adipose tissue or cervical adipose tissue may compress the airway when the tonic electrical activity of the pharyngeal muscles decreases with sleep onset. Data reviewed support the idea that the upper airway of OSA patients may be more collapsible than the upper airway of nonapneic subjects. Intrinsic tissue abnormalities have not been demonstrated that might be responsible for this collapsibility. Changes in collapsibility found are consistent with, and may be due to, changes in tonic and phasic contraction of upper airway muscles. Abnormalities in reflexes affecting upper airway size surely might exist in OSA. Edema or inflammation of pharyngeal tissues might not only narrow the upper airway but might also impair normal function of the receptors responsible for initiating protective reflexes. We propose the fluctuation between a low- and a high-drive state contributes to upper airway collapse in OSA. With this fluctuation the balance of forces and critical pressure concepts discussed above come into play (Fig 6). By stimulating upper airway inspiratory muscles, CO2 eliminates the hypoapneic, low-drive, high-resistance periods and thereby reduces the number of apneas. In addition, preferential stimulation of upper airway muscle activity dilates the upper airway per se. If the relative value of each of these factors can be determined diagnostically, perhaps therapy can be made more specific. By being more specific, therapy should be more successful than the present practice of prescribing a particular therapy, regardless of the specific mechanism responsible for the OSA in a given patient.
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PMID:Mechanisms of obstructive sleep apnea. 820 24

From August 1990 to August 1991, sixteen patients with bullae or blebs (pneumothorax 9, giant bullae 5, bullous emphysema 2) were treated by CO2 laser ablation under limited thoracotomy. We found the irradiation of bullae or blebs by CO2 laser quite effective in eliminating these bullous lesions which were often multiple and inoperable by conventional methods. Histological examination revealed the wall of bullae where CO2 laser was applied became thick with dense fibrous tissues and degenerated collagen fibers which, however, were not disrupted. The procedure was safe and we were able to operate patients with disabling emphysema. Because CO2 laser can penetrate only 0.2-0.3 mm of tissue thickness, it is suitable for the ablation of bullous lesions which have thin walls and rapidly shrink and collapse by irradiation leaving thick walled scar tissues. Removing multiple bullae and blebs in patients with bullous emphysema can improve gas exchange by reducing dead spaces and elevating the diaphragm which is often flat and downward displaced because of hyperinflation in these patients. We are planning to incorporate thoracoscopy for this operation to make the procedure less invasive.
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PMID:[Application of laser in the treatment of spontaneous pneumothorax and emphysema]. 173 44

Hysteroscopy and laparoscopy are relatively non-invasive methods routinely employed in the investigation of infertility. The danger of air embolism during these procedures was recognized early, and carbon dioxide was substituted for air since it is more readily soluble in blood. In this report we describe 3 cases of circulatory collapse and cardiac arrest in healthy young women during routine hysteroscopy (out of a total of 62 patients during the period 1989-1990) which were most probably caused by massive carbon dioxide embolism. Premedication was with oral diazepam 10 mg. Anesthesia was induced with 0.1 mg fentanyl, 2.5 mg droperidol and 100 mg methohexital (100 mg propofol in one case). Intubation was facilitated with 2 mg pancuronium and 50-100mg succinylcholine. Anesthesia was maintained with nitrous oxide 66% and halothane. Ventilation was controlled with a tidal volume of 10 ml per kilogram body weight at a rate of 10 per minute. Monitoring included ECG, automated non-invasive blood pressure, capnometry, pulse oximetry and body temperature. Anesthesia was uneventful prior to insufflation. In each case the signs and symptoms began approximately 5-8 minutes after the start of insufflation and consisted of an initial tachycardia rapidly followed by ventricular dysrhythmias, bradycardia and cardiac arrest. The end-tidal CO2 decreased during the tachycardic phase and prior to asystole. The patients were cyanotic with engorged jugular veins. Resuscitation with closed chest heart massage and intravenous epinephrine or orciprenaline was successful in every case. The typical "mill wheel phenomenon" of gas embolism was audible on auscultation after heart activity had returned, but disappeared after about 5 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Gas embolism with cardiac arrest during hysteroscopy. A case report on 3 patients]. 177 42

The treatment of hyperthermia produced by passive warming was studied in anesthetized rats weighing 250-300 grams. In the first set of seven experiments, the authors found that venous blood oxygen fell as core temperature rose. Intraperitoneal injection of 20 ml of the oxygen carrying fluorocarbon (perfluorotributylamine, FC-43) emulsion in three of the animals shifted the curve to the right improving venous oxygen content (p less than 0.1). In the second series of experiments, a catheter was placed in the carotid artery. This catheter was attached to a pressure transducer for continuous recording of blood pressure and heart rate. Periodic blood samples were removed for measurement of blood gases, pH, and lactate. Four of the animals received 20 ml of isotonic saline, three received 20 ml of FC-43 emulsion both given intraperitoneally, and four served as controls. In the control group, there was an increase in systolic blood pressure and heart rate which peaked at a colon temperature of 42 degrees C, followed by cardiovascular collapse and death around 43 degrees C. Arterial PO2 (corrected for temperature) remained relatively constant up to 42 degrees C, and then fell. The arterial PCO2 rose sharply when the core temperature exceeded 43 degrees C. Arterial lactate content began to increase at 42 degrees C and above 43 degrees C was 2.5 fold elevated. Isotonic saline provided circulatory support but did not change the hypoxia or mixed acidosis from CO2 and lactate above 43 degrees C. FC-43 emulsion decreased hypoxia and improved circulatory performance but was associated with a mild respiratory alkalosis as arterial PCO2 fell.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental hyperthermia: protective effect of oxygen carrying fluorocarbon and crystalloids intraperitoneally. 189 82

Experiments were designed to determine the role of the endothelium in response to hypoxia in the human internal mammary artery (IMA). Segments of IMA were harvested during coronary artery bypass surgery. Rings (4 mm in length) of IMA, with and without endothelium, were suspended to force transducers in organ baths containing a physiologic salt solution (37 degrees C, 95% O2/5% CO2, and pH = 7.4). The rings were contracted with norepinephrine (NE, 1 x 10(-7) M, initial tension), and then exposed to hypoxia (95% N2/5% CO2, PO2 = 35 +/- 5 mmHg). In IMA segments with endothelium, hypoxia caused an initial, transient relaxation (hypoxic inhibition) to 52 +/- 9% of the initial tension, followed by contraction of the blood vessel (hypoxic potentiation; 178 +/- 10% of initial tension). In vessels without endothelium, hypoxia only induced relaxation (to 10 +/- 2% of initial tension). In vessels with endothelium, reoxygenation induced transient rapid relaxation (to 31 +/- 12%; post-hypoxic inhibition) which then stabilized to 50 +/- 14% of the initial tension. However, segments without endothelium returned to their initial tension. Indomethacin (1 x 10(-5) M) reduced the endothelium-dependent hypoxic contraction and abolished the hypoxic and post-hypoxic inhibition. Free radical scavengers (superoxide dismutase plus catalase and deferoxamine) did not modify the responses to hypoxia and reoxygenation. These experiments indicate that hypoxia induces the release of an endothelium-derived constricting cyclooxygenase product from the human IMA endothelium, and that reoxygenation causes release of a cyclooxygenase-dependent endothelium-derived relaxing factor. The release of endothelium-derived constricting factor(s) could induce vasospasm and cause cardiovascular collapse if IMA grafts are exposed to hypoxia perioperatively.
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PMID:Vasoconstriction to hypoxia of the human internal mammary artery. 193 21

Acquired bronchial stenosis following prolonged endotracheal intubation is uncommon, but in infants it is associated with significant morbidity. A variety of endobronchial techniques including forceps or cautery resection and balloon dilatation have been used with inconsistent results. Laser therapy seems attractive, but pediatric applications have been very limited. We report the first series of infants with life-threatening acquired bronchial stenosis treated with an argon laser. Eight infants, age 3 weeks to 2 years, presented with symptomatic bronchial obstruction following prolonged intubation. Seven of these patients had at least 90% obstruction of a lobar or mainstem bronchus. Under general anesthesia a 300 or 600 micron quartz laser fiber was passed through the suction channel of a 3.5-mm flexible or 3-mm rigid bronchoscope. The laser was operated at 2.5 to 3.5 W in 0.5-second pulses, to ablate the obstructing tissue. Multiple procedures, spaced no closer than 10 days, were required in three of eight infants. Follow-up bronchoscopy after 2 to 30 months revealed normal findings in five of eight infants. All but one child, who has persistent collapse of the bronchus intermedius due to bronchomalacia at the site of the obstruction, had satisfactory results. The only complication was a pneumothorax in a 1,300 g infant, which developed eight hours after treatment. Our experience suggests that the argon laser is effective in the management of endobronchial lesions in infants and is superior to the CO2 and Neo-dymium-yttrium aluminum garnet (Nd-YAG) lasers for this purpose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acquired symptomatic bronchial stenosis in infants: successful management using an argon laser. 229 42

Local hemodynamics were investigated during nine operations for spinal dural arteriovenous (AV) fistulas. In eight cases, microvascular Doppler sonography was used to measure flow velocities and vasomotor reactivity to CO2 changes. Intravascular pressure recordings of the draining veins on the medullary surface were performed in nine cases. The flow velocities in dural AV fistula feeding vessels were not as high as has been shown in cerebral angioma feeders. The AV fistula feeders often showed low end-diastolic flow velocities as a sign of increased vascular resistance, even in the presence of a downstream AV fistula, thus proving disturbance of venous outflow from the spinal canal. After excision of the fistula, the circulation of the spinal cord vessels improved, with higher inflow and outflow velocities. In the veins formerly draining the fistula, no further flow could be recorded; however, they did not collapse, indicating that some pressure remained. The mean venous pressure in the dural AV fistulas was about 74% of the systemic arterial pressure. It increased concomitantly with the arterial pressure, which may explain the clinical deterioration that occurs during physical activity. Fistulas with a high shunt volume on angiography showed only moderately increased venous pressures and a more pronounced pressure drop compared to low-volume fistulas. The CO2 reactivity of vessels supplying the spinal cord could be demonstrated in all cases, and was normal before and after removal of the fistula.
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PMID:Hemodynamics of spinal dural arteriovenous fistulas. An intraoperative study. 249 95

The upper airway (UAW) is intrinsically unstable and susceptible to collapse when the negative inspiratory intraluminal pressure exceeds the stabilizing forces which prevent obstruction. In the present study we evaluated mechanisms by which UAW patency is maintained in the presence of increased inspiratory flows when respiration is stimulated. In seven anesthetized dogs breathing spontaneously through a low tracheostomy, the UAW was isolated by a second tracheostomy directed rostrally. UAW pressure-flow relationship and stability against collapse were evaluated during steady flow in the inspiratory direction while the animals were breathing 100% O2 or a hypercapnic gas mixture. The pressure-flow curves of the isolated UAW demonstrated the characteristic pattern of collapsible tubes. Steady state hypercapnia resulted in lower UAW resistance during both inspiration and expiration. UAW resistance decreased linearly as PCO2 and ventilation increased over the course of CO2 rebreathing. In addition, during hypercapnia the critical negative intraluminal pressure required to induce UAW collapse and obstruction increased from -4.3 +/- 0.9 to -8.5 +/- 1.5 SE cm H2O (p less than 0.01), indicating increased stability of the UAW. Since hypercapnia is known to stimulate UAW muscles, our findings suggest that increased UAW muscle activity improves UAW patency both by decreasing their resistance to airflow, and by increasing UAW walls rigidity and stability against collapse.
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PMID:Effect of hypercapnia on upper airway resistance and collapsibility in anesthetized dogs. 249 2


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