Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 46-year-old man underwent cosmetic facial surgery under general anesthesia. He was ventilated by mask with an oxygen-enriched gas mixture for 4 to 6 h and monitored by pulse oximetry. Despite adequate arterial saturation (SaO2 > 90 percent) throughout the procedure, he remained in a deep coma after termination of anesthesia. Initial arterial blood gas analysis revealed a pH of 6.60 and a PaCO2 of 375 mm Hg. The patient was intubated and placed on mechanical ventilation. As his respiratory acidosis resolved, he regained consciousness quickly and recovered without any neurologic deficits. This case of record extreme hypercapnia and review of the literature demonstrates that survival is possible in acute severe respiratory acidosis as long as tissue anoxia and ischemia are prevented. We discuss the tissue effects of acute hypercapnia and newer aspects of the nature of intracellular pH regulation in critical tissues that afford considerable tolerance to acidosis. The dependence of these mechanisms upon active ion transport underscores the importance of adequate tissue oxygenation and perfusion.
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PMID:Resuscitation from severe acute hypercapnia. Determinants of tolerance and survival. 144 82

A study of the duration of analgesia and of the respiratory response to hypercapnia was carried out in 14 children who had had a caudal block with either bupivacaine alone (group B) or combined with fentanyl (Group B+F). Fourteen ASA I or II 5 to 10-year-old children undergoing genital and urinary surgery were included. They were not premedicated. At first, general anaesthesia was induced with halothane and nitrous oxide in oxygen. Thereafter, caudal anaesthesia was then carried out with 1 ml.kg-1 of 0.25% bupivacaine with adrenaline 1 in 200,000. Group B+F patients were also given 1 microgram.kg-1 of fentanyl in 1 ml of normal saline, and those in Group B 1 ml of normal saline. The level of sensory loss on leaving the operating theatre as well as the duration of motor paralysis were monitored. Postoperative pain was scored with Hannalah and Broadman's score (0 to 10) 2, 4, 8 and 24 h after the caudal block. Respiratory rate (fR), tidal volume (VT) and minute ventilation (VE) were assessed 10 min before induction of general anaesthesia, and 30, 60 and 120 min after the caudal anaesthesia. Petco2 was also measured before induction of general anaesthesia, and 60 and 120 min after caudal anaesthesia; at the same times, the ventilatory response to hypercapnia was assessed using Read's method with a Douglas bag containing 7% CO2 and 93% O2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Caudal block in children: analgesia and respiratory effect of the combination bupivacaine-fentanyl]. 150 85

A healthy young woman suffered cardiac arrest during diagnostic laparoscopy; emergent laparotomy was required to release the pneumoperitoneum and reinitiate cardiac rhythm. Several cases of cardiovascular collapse have been described in the literature. Possible causes for such complications include hypercapnia or anoxia from hypoventilation during anesthesia, decreased venous return and cardiac output secondary to elevated intra-abdominal pressure, gas embolism, and a profound vagal response to peritoneal distention. Treatment includes cardiovascular support and rapid release of the pneumoperitoneum.
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PMID:Asystolic cardiac arrest: a rare complication of laparoscopy. 153 24

Human upper airway dilator muscles are clearly influenced by chemical stimuli such as hypoxia and hypercapnia. Whether in humans there are upper airway receptors capable of modifying the activity of such muscles is unclear. We studied alae nasi electromyography (EMG) in normal men in an attempt to determine 1) whether increasing negative intraluminal pressure influences the activity of the alae nasi muscle, 2) whether nasal airway feedback mechanisms modify the activity of this muscle, and 3) if so, whether these receptor mechanisms are responding to mucosal temperature/pressure changes or to airway deformation. Alae nasi EMG was recorded in 10 normal men under the following conditions: 1) nasal breathing (all potential nasal receptors exposed), 2) oral breathing (nasal receptors not exposed), 3) nasal breathing with splints (airway deformation prevented), and 4) nasal breathing after nasal anesthesia (mucosal receptors anesthetized). In addition, in a separate group, the combined effects of anesthesia and nasal splints were assessed. Under each condition, EMG activity was monitored during basal breathing, progressive hypercapnia, and inspiratory resistive loading. Under all four conditions, both load and hypercapnia produced a significant increase in alae nasi EMG, with hypercapnia producing a similar increment in EMG regardless of nasal receptor exposure. On the other hand, loading produced greater increments in EMG during nasal than during oral breathing, with combined anesthesia plus splinting producing a load response similar to that observed during oral respiration. These observations suggest that nasal airway receptors have little effect on the alae nasi response to hypercapnia but appear to mediate the alae nasi response to loading or negative airway pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of control of alae nasi muscle activity. 156 88

Problems facing a patient with severe dyspnea secondary to diaphragmatic herniation are hypoxia, hypercarbia and respiratory acidosis, and cardiovascular instability. It is easy to precipitate a crisis in these patients during anesthetic induction as a result of stress, bad positioning, induction of pneumothorax, or inappropriate anesthetic technique. These patients require a smooth, stress-free perianesthetic period with preoxygenation, positioning with the affected side down, rapid intravenous induction, endotracheal intubation, and mechanical ventilation. Maintenance with isoflurane is preferred, and nitrous oxide should be avoided. Close monitoring of the cardiovascular and pulmonary systems is essential. Recovery from anesthesia should include oxygen supplementation, pleural drainage, and local analgesia if required.
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PMID:Anesthesia for patients with diaphragmatic hernia and severe dyspnea. 158 3

To evaluate adequate anesthetic depth without unacceptable respiratory consequences during total propofol intravascular anesthesia without intubation, the respiratory response was studied in 20 healthy patients (ASA class I or II), aged 20-50, premedicated with fentanyl 2 micrograms/kg. Anesthesia was induced in all patients with propofol 2.5 mg/kg, subsequently maintained by continuous propofol infusion at 12 mg/kg/h. An additional bolus of 20-60 mg propofol was given when anesthesia was considered inadequately. Assisted ventilation with 100% oxygen through a face mask was applied when apnea time was longer than 60 s. The mask was removed when patients regained spontaneous breathing. During induction stage, 7 patients developed apnea which required ventilatory support, although the period of apnea was short. Among them four regained spontaneous breathing within 5 min, and three within 10 min. PaCO2 significantly increased at both 10 min and 20 min after induction as compared with those before induction (p less than 0.05), while the change between 10 min and 20 min after induction was not statistically different. PaO2 showed little change and also it was not statistically significant. During maintenance of anesthesia spontaneous ventilation was stable and adequate. Though mild hypercapnia was noted, no medication was necessary. There was no episode of arterial oxygen desaturation throughout the course of maintenance. All patients could be adequately anesthetized except for six patients who required additional dose for insufficient anesthetic depth. No major adverse reactions occurred during or after induction. We concluded that the respiratory effect of propofol in total intravenous anesthesia could be divided into two stages: the induction stage and the maintenance stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of total intravenous propofol on spontaneous respiration during anesthesia for minor surgery. 160 23

Surgical stress and general anesthesia can suppress immune function and thus may increase postsurgical infections and tumor metastasis. We previously reported that two narcotics commonly used in high-dose opiate anesthesia (fentanyl and sufentanil) suppress natural killer (NK) cell activity in rats. Such doses of narcotics also cause respiratory depression accompanied by hypoxia, hypercarbia, and acidosis, which might account for the observed narcotic-induced NK suppression. In the present study, we compared the effects of fentanyl on NK activity in ventilated and non-ventilated rats. Fentanyl significantly suppressed NK cell activity to the same magnitude in the two groups, although the groups significantly differed in CO2 and O2 levels. The fact that high-dose fentanyl-induced NK suppression can be demonstrated in ventilated rats accentuates the relevance of these findings to clinical studies showing NK suppression in the immediate postoperative period. Such immunosuppression could be a risk factor for patients undergoing surgery, especially in cancer-related operations.
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PMID:Narcotic-induced suppression of natural killer cell activity in ventilated and nonventilated rats. 164 47

Breathing is impaired by the loss of wakefulness that accompanies sleep, certain comatose states, and anesthesia. Although state-dependent decrements in breathing and the ability to respond to hypercapnic stimuli are characteristic of most mammals, the neural mechanisms that cause state-dependent changes in respiratory control remain poorly understood. The present study examined the hypothesis that cholinergic mechanisms in the medial pontine reticular formation (mPRF) can cause state-dependent changes in breathing and in the hypercapnic ventilatory response (HCVR). Six cats were anesthetized with halothane and chronically instrumented for subsequent studies of breathing during wakefulness, non-rapid-eye-movement (NREM) sleep, rapid-eye-movement (REM) sleep, and during the REM sleep-like state caused by mPRF microinjections of carbachol or bethanechol. Minute ventilation was significantly decreased during the carbachol-induced REM sleep-like state (DCarb) compared with wakefulness. The HCVR in NREM, REM, DCarb, and after bethanechol was less than the waking HCVR. These results show for the first time that cholinoceptive regions in the mPRF can cause state-dependent reductions in normocapnic minute ventilation and in the ventilatory response to hypercapnia.
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PMID:Cholinergic reticular mechanisms influence state-dependent ventilatory response to hypercapnia. 167 9

Patients with cardiopulmonary insufficiency undergoing laparoscopic surgery with carbon dioxide (CO2) pneumoperitoneum may retain CO2 resulting in clinically significant respiratory acidosis. A canine model of pulmonary emphysema induced by papain inhalation was utilized to evaluate the respiratory effects of both CO2 and helium pneumoperitoneum. Prior to papain inhalation and 5 and 8 weeks after initial treatment under general anesthesia, mechanical ventilation was adjusted to maintain the end-tidal CO2 (ETCO2) at 40 mm Hg during baseline and pneumoperitoneum physiologic monitoring periods. Utilizing an analysis of variance, hemodynamic and respiratory physiologic parameters were compared. In this canine model, all dogs demonstrated consistent hypercarbia during CO2 pneumoperitoneum prior to papain treatments, but CO2 retention was significantly increased in the emphysematous state. The occurrence of hypercarbia during CO2 pneumoperitoneum may be underestimated by ETCO2 monitoring as was revealed by an increased PaCO2 (arterial carbon dioxide pressure)-ETCO2 gradient with an increasing time interval between papain exposure and period of physiologic monitoring. Irrespective of the pulmonary condition of the dog, helium pneumoperitoneum did not produce any hypercarbic or acidic changes when compared with the concomitant baseline period of dogs prior to the induction of pneumoperitoneum, thus suggesting that helium pneumoperitoneum may be a reasonable alternative in patients at risk for CO2 retention.
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PMID:Hypercarbia during carbon dioxide pneumoperitoneum. 173 68

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
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PMID:Acute postoperative hypertension in the hypertensive patient. 173 70


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