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)

Panic disorder (PD) is a complex condition that is further complicated by its numerous inducers, which include hypercapnia, hypoxia, sodium lactate, caffeine and cholecystokinin. It seems unlikely that there are specific suffocation receptors for each of these inducers in the brain. The pulmonary neuroepithelial bodies (NEBs), which are situated at the bifurcation point of the small bronchi, act as storage cells for 5-hydroxytryptamine (5-HT) and sensors for suffocation. If we suppose that PD might represent an inflammation of the NEBs, bradykinin (BK) which augments the airway hyper-response to diverse indcers might cause these cells to release 5-HT along with peptides and panneuroendcrine markers from their dence-core secretory granules. It was revealed that BK with 5-HT could cross the blood-brain barrier (BBB). When 5-HT released from these cells along with BK cross the BBB, the release of 5-HT at the axonal terminals in the serotonergic neurons in the brain will be inhibited, since the 5-HT1 autoreceptor have a higher affinity for 5-HT than do the 5-HT2 receptors. The inhibition of 5-HT at the axonal terminal causes to suppress the periaqueductal gray matter, which inhibits flight reactions to impending danger, pain or asphyxia. In short, this serotonergic situation might bring about PD. According to this theory, the type of inducer that the PD patient is exposed to is unimportant as long as it stimulates the NEBs, and through the effect of 5-HT and BK, PD would be revaluated as a somatic disease that directly and reversibly affects the brain.
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PMID:Novel hypothesis for the cause of panic disorder via the neuroepithelial bodies in the lung. 1582 15

Ischemic pain occurs when there is insufficient blood flow for the metabolic needs of an organ. The pain of a heart attack is the prototypical example. Multiple compounds released from ischemic muscle likely contribute to this pain by acting on sensory neurons that innervate muscle. One such compound is lactic acid. Here, we show that ASIC3 (acid-sensing ion channel #3) has the appropriate expression pattern and physical properties to be the detector of this lactic acid. In rats, it is expressed only in sensory neurons and then only on a minority (approximately 40%) of these. Nevertheless, it is expressed at extremely high levels on virtually all dorsal root ganglion sensory neurons that innervate the heart. It is extraordinarily sensitive to protons (Hill slope 4, half-activating pH 6.7), allowing it to readily respond to the small changes in extracellular pH (from 7.4 to 7.0) that occur during muscle ischemia. Moreover, both extracellular lactate and extracellular ATP increase the sensitivity of ASIC3 to protons. This final property makes ASIC3 a "coincidence detector" of three molecules that appear during ischemia, thereby allowing it to better detect acidosis caused by ischemia than other forms of systemic acidosis such as hypercapnia.
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PMID:An acid-sensing ion channel that detects ischemic pain. 1625 23

As the number of elderly patients undergoing surgery continues to rise, it is important to consider anaesthetic options that minimize physiological stress in these patients. Monitored anaesthesia care (MAC), or sedation and monitoring during surgery, is an attractive option for certain common procedures. However, those administering MAC must consider the normal decline in functional reserve in patients aged >70 years. This includes loss of normal compensation for the stress of hypovolaemia, decreased peripheral vascular resistance, altered mental status and reduced response to hypoxia and hypercarbia associated with the perioperative and sedated state in this population. In addition, vigilance is necessary to identify co-morbid states, which increase in incidence with age and often present atypically. Elderly patients have increased sensitivity to all sedatives and opioids (doubled by age 80 years, quadrupled by age 90 years with benzodiazepines). As a result of changes in body composition, as well as senescence of renal and hepatic function, the time to onset and offset of even short-acting sedatives will be prolonged. There is also extreme variability in the response to sedatives among these patients. Anaesthetic dosing should be in smaller increments in the elderly, boluses reduced by half and infusions reduced by as much as two-thirds. Caution must be exercised through full monitoring of intra-operative and postoperative mental status, oxygenation and perfusion states. Pain is best treated using smaller doses in a multimodal regimen, the aim being to reduce adverse effects while ensuring adequate pain relief. In this way, a huge range of procedures can be safely performed in our aging population with expectations for a full and early return to baseline functional status.
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PMID:Monitored anaesthesia care in the elderly: guidelines and recommendations. 1854 Jun 88

The presence of pulmonary arterial hypertension (PAH) is a significant predictor of major perioperative cardiovascular complications in patients undergoing cardiac diagnostic or interventional procedure or non cardiac surgery under sedation and/or anesthesia. Factors that precipitate a pulmonary hypertensive crisis include hypoxia, hypercarbia, acidosis, hypothermia, pain and airway manipulations. Pain management is challenging in patients with significant PAH. We report the use of dexmedetomidine for sedation and analgesia in a 16 year old patient with significant pulmonary hypertension, pneumonia and impending cardiorespiratory failure. This resulted in avoidance of endotracheal intubation and positive pressure ventilation, with subsequent recovery to discharge home.
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PMID:Novel use of dexmedetomidine in a patient with pulmonary hypertension. 1854 49

This review discusses headaches secondary to disorders of homeostasis, formerly known as "headaches associated with metabolic or systemic diseases." They include the headaches attributed to 1) hypoxia and/or hypercapnia (high altitude, diving, sleep apnea); 2) dialysis; 3) arterial hypertension; 4) hypothyroidism; 5) fasting; and 6) cardiac cephalalgia. For each headache type, we discuss the clinical features and diagnosis, as well as therapeutic strategies.
Curr Pain Headache Rep 2008 Aug
PMID:The metabolic headaches. 1862 7

Inhibition of ventilatory drive may improve the sensation of dyspnea, because heightened ventilatory demand contributes to dyspnea. Tris-hydroxymethyl aminomethane (THAM) is an alkalizing agent that does not increase CO(2) production and exerts a depressant effect on respiration. The purpose of this study was to clarify the effect of THAM on dyspnea associated with increases in respiratory drive. We investigated the effects of THAM on dyspneic sensation produced by a combination of hypercapnia (mean PaCO(2)=52 mm Hg) and elastic loading (30 cm H(2)O/L) in 14 healthy subjects. The subjects were asked to rate their dyspneic sensation using a visual analogue scale (VAS) during the loaded breathing while monitoring ventilation using a pneumotachograph. THAM was infused at a rate of 0.4 mL/kg/minute for 10 minutes, and the effects of THAM on dyspnea and ventilation were evaluated by comparing the steady-state values of ventilatory variables and VAS score obtained before and after THAM administration. Administration of THAM corrected respiratory acidosis and was associated with significant improvements in VAS score and significant decreases in minute ventilation, respiratory frequency, and ventilatory drive. THAM administration greatly alleviates dyspneic sensation associated with the increase in respiratory drive and could be an effective therapy for treating severe dyspnea in patients with hypercapnia.
J Pain Symptom Manage 2009 Feb
PMID:THAM improves an experimentally induced severe dyspnea. 1880 42

Dyspnea is the unpleasant awareness of breathing while healthy persons will hardly sense their own breath at rest. Dyspnea is comparable to pain because both caution the organism that will activate protective mechanisms to avoid further damage. Dyspnea results from central nervous processing of respiratory feed back signals. Feed back from respiratory muscles, the chest wall, the airways and the lung reach the brain while partial pressure of oxygen and carbon dioxide is continuously monitored and arterial blood gases are permanently stabilized. Sensation of breathlessness depends on its origin. Main qualities of dyspnea include air hunger during hypercapnia, laboured breathing during increased minute ventilation and chest tightness in asthma. During chronic dyspnea, respiratory control aims for a new breathing pattern that will ease breathlessness. Since respiratory control includes both autonomic regulation and cortical modulation of breathing, voluntarily guided respiration can be employed to influence other autonomic regulated systems and pain perception.
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PMID:[Breathlessness: different causes and qualities of dyspnea]. 1955 55

Red blood cells from patients with sickle cell disease will sickle under conditions of hypoxemia and acidosis which is a similar milieu found in malignant tumors. While control of tumor angiogenesis has long been a goal of cancer therapy, selective occlusion of tumor blood supply may be achieved by transfusion of sickle cells into patients who suffer metastatic cancer. Although this potential therapy has not been previously reported in the medical literature, the concept may have been elusive to medical mainstream thinking because it requires transfusion of diseased cells. For this therapy to be effective, other environmental factors may need to be manipulated such inducing mild hypoxemia or hypercarbia (respiratory acidosis) to induce red cell sickling. Preliminary evidence supportive of this therapeutic approach to cancer treatment is provided by case evidence that sickle cell occlusion of a malignant brain tumor (glioma) produced tumor necrosis. Also sickle cells have been successfully transfused into primates. Furthermore, donor blood is crossmatched and transfused into patients suffering from sickle cell disease regularly in clinics and this procedure is associated with acceptable morbidity. Most importantly, animal models of sickle cell disease and cancer currently exist, and this theory could be tried with available technologies including ultrasound detection of vaso-occlusion. While the proposed therapy may not cure metastatic cancer, this treatment could prove useful for decreasing the size and perhaps the pain from metastatic tumor burden. Therefore, it is hypothesized that ABO Rh compatible crossmatched sickle cells transfused into patients who suffer metastatic cancer under controlled conditions of blood oxygenation and pH will selectively produce vaso-occlusive infarcts in malignant tumors and be a useful therapy. The author hopes for further investigations.
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PMID:Transfusion of sickle cells may be a therapeutic option for patients suffering metastatic disease. 2044 56

Sedation for gastrointestinal endoscopy may induce central respiratory depression and/or airway obstruction. Early diagnosis and treatment of these complications is mandatory as the resulting hypoxia may cause irreversible damage, particularly to vital organs, or death. Sedatives and centrally acting analgesics depress respiration in a dose-dependent manner. However, significant untoward events are preventable by titrating the doses for sedation and by monitoring patient oxygenation and respiration. Cardiovascular adverse events may also occur during gastrointestinal endoscopy, and can be major or minor. Hypotension needs treatment as well as severe hypertension. Cardiac dysrhythmias may occur due to stress, pain and/or hypercarbia, which may accompany endoscopies. The anesthesia provider must be able to diagnose, assess the risk and treat all the adverse events during gastrointestinal endoscopy. The resuscitation equipment, including the defibrillator, must be readily accessible.
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PMID:Emergencies and treatment of complications. 2040 54

In the neonatal population, pleural effusion and particularly tension pneumothorax can be a deadly situation. Pneumothorax occurs more often in the neonatal period that any other time of life. Tension pneumothorax can result in very high pressures within the pleural space, collapsing the lung on the involved side and resulting in immediate hypoxia, hypercapnia and subsequent circulatory collapse. For these reasons, the ability to recognize, understand and treat these pathologies is essential for neonatal health and a good outcome. Neonates have many factors that can contribute to. these problems. These include respiratory distress syndrome, mechanical ventilation, sepsis, pneumonia, aspiration of meconium, congentital malformation, hydrothorax, congenital or acquired chylothorax. The diagnosis can be made by clinical examination, transillumination (pneumothorax) and chest x-ray. Besides, lung ultrasound constitutes a visual medicine and provides a transparent approach to the acutely ill patient, newborn included, guiding diagnosis, management and care. Newborns with moderate to severe symptoms and those receiving positive pressure ventilation require tube thoracostomy. If a tension pneumothorax is suspected, emergency needle decompression in the second intercostal space in the midclavicular line is required. In this article, we describe the management of tube thoracostomy using trocar tubes or pigtail catheters. Besides, we pay attention to the use of pain control for neonates undergoing painful procedures such as chest tube insertion.
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PMID:[Management of pleural drainage]. 2109 89


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