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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Continuous monitoring of the cerebral blood flow, oxyhemoglobin, deoxyhemoglobin, total hemoglobin, oxidized cytochrome a, a3, and tissue pH during prolonged CO2 or N2 loading in 2-week-old rabbits was performed by near-infrared spectroscopy, the thermocouple method, and a tissue pH meter. Near-infrared spectroscopy demonstrated decreases in oxyhemoglobin and oxidized cytochrome a, a3 and increases in deoxyhemoglobin and total hemoglobin in the early stage within 5 min, which gradually lessened with time on both 10% concentration of inspired O2 with CO2 and N2. CBF increased with venous retention in the early stage and then slowly decreased in parallel with blood pressure and oxidized cytochrome a, a3 on abolition of autoregulation. These changes were more remarkable during the 10% concentration of inspired O2 with CO2 than N2 which may be caused by marked acidosis and hypotension associated with hypercarbia. Oxidized cytochrome a, a3, however, demonstrated a gradual decrease in 10% concentration of inspired O2 with N2 rather than CO2; therefore, the continuous monitorings demonstrated hemodynamic and oxygenation changes despite the same extent of prolonged hypoxic loading. These changes in prolonged hypoxic conditions may occur in human intrapartum asphyxia which develops into postnatal hypoxic-ischemic encephalopathy.
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PMID:Monitoring of immature rabbit brain during hypoxia with near-infrared spectroscopy. 155 75

The management of children with severe acute asthma who required admission to the intensive care (ICU) of this hospital during 1982 to 1988 was reviewed retrospectively. A total of 89 children were admitted to the ICU on 125 occasions. During the study period, 24% of the patients were admitted to the ICU on more than one occasion. Prior to admission to this hospital, patients had been symptomatic for a mean of 48 hours. Although all patients had received bronchodilators before admission to hospital, only 23% of patients had received oral corticosteroids. According to initial arterial blood gas values determined in the ICU, 77% of the patients had hypercapnia (PaCO2 greater than 45 mm Hg). The pharmacologic agents used in the ICU included nebulized beta 2-agonists (100% of admissions), theophylline (99%), steroids (94%), nebulized ipratropium bromide (10%), IV albuterol (38%), and IV isoproterenol (10%). Mechanical ventilation was necessary in 33% of admissions; the mean duration of ventilation was 32 hours. Ten patients had pneumothorax; in six cases, these were related to mechanical ventilation. Three of the patients who received mechanical ventilation died, representing a mortality of 7.5%. In each of these patients, sudden, severe asthma episodes had developed at home, resulting in respiratory arrest. They had evidence of hypoxic encephalopathy at the time of admission to the ICU and eventually were declared brain dead. It was concluded that delay in seeking medical care and underuse of oral corticosteroids at home may have contributed to the need for ICU admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Severe acute asthma in a pediatric intensive care unit: six years' experience. 231 83

Eleven observations of severe multicystic encephalopathy ( MCE ) in young infants and in a two-year-old child provide the basis for a summing-up and discussion of the various aspects of this characteristic polyetiologic phenomenon occurring in early infancy. In all cases the triggering causes or underlying disorders were different, although in five cases the common pathogenetic mechanism was a disturbance of circulation and/or respiration (acute respiratory distress syndrome). In two cases the basic disorders were a suppurative and a granulomatous meningoencephalitis. Carbon monoxide poisoning had occurred in one and diffuse meningocerebral angiomatosis in another two cases. In the eleventh case, one of a complicated twin birth, the exact cause of the MCE remained obscure. These cases together with those recorded in the literature demonstrate that the surprisingly constant pattern of damage in MCE , which results from different etiologic conditions, should be due to a specific mode of reaction of the infantile brain to a common pathogenetic mechanism. Anoxia with hypercapnia and the formation of brain edema are discussed as the basic events in the pathogenesis of MCE .
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PMID:Multicystic encephalopathy--a polyetiologic condition in early infancy: morphologic, pathogenetic and clinical aspects. 632 15

Over an 18-month period, 56 pediatric patients who sustained severe neurologic insults underwent intracranial pressure (ICP) monitoring. Indications for monitoring ICP were (1) a Glasgow Coma Scale (GCS) score of 7 or less or (2) loss of consciousness with inability to utter recognizable words or follow commands. Diagnoses were head trauma (n = 40), Reye's syndrome (n = 10), and hypoxic encephalopathy due to near-drowning (n = 6). Eighty per cent of patients had ICP elevations requiring treatment. The complication rate was 5.3 per cent, with no serious complications or infections noted. Overall mortality was 14 per cent, but patients with hypoxic encephalopathy had significantly higher mortality (33%) when compared to patients with head trauma (12.5%) or Reye's syndrome (10%). Other factors associated with a poor outcome included presence of an intracranial mass lesion, GCS score, ICP elevations, hypoxemia, hypotension, hypercarbia, and the presence of multiple injuries (p less than 0.01). Early diagnosis and aggressive treatment in these patients, including the use of ICP monitoring, has resulted in acceptable recovery in over 85 per cent of these patients.
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PMID:Emergency intracranial pressure monitoring in pediatrics: management of the acute coma of brain insult. 708 9

Intracellular pH and ammonium ion concentration are potent modulators of cerebral amino acid metabolism. Furthermore, intracellular acidosis and hyperammonemia accompany conditions such as ischemic encephalopathy and seizures and may contribute to the pathological sequelae observed. In vivo NMR spectroscopy permits multiple, non-destructive measurements of important cerebral metabolic intermediates in the same animal. We describe here the use of 1H, and 31P NMR spectroscopy to investigate the effects of acute changes in intracellular pH and ammonium ions on cerebral glutamate, glutamine, and lactate levels in vivo. We then show how 1H NMR can be used to indirectly follow the flow of 13C label from [1-13C] glucose into the cerebral glutamate pool, allowing us to measure cerebral TCA activity in normal and chronically hyperammonemic rats. Male Sprague-Dawley rats (160-210 gm), fasted 24-hours, were tracheotomized, paralyzed and ventilated on 30% O2/70% N2O. NMR spectroscopy was performed at a field strength of 8.4 Tesla using a Bruker AM-360 wide bore spectrometer. An elliptical surface-coil (8 x 12 mm) was double-tuned to either the 1H and 31P or 1H and 13C frequencies. After retraction of extracranial tissues, the coil was positioned over the skull 2 mm posterior to the bregma. Tail arteries and veins were cannulated allowing periodic measurements of PO2, pCO2, pH and glucose in arterial blood and intravenous infusions. Respiratory acidosis was induced in rats by the addition of CO2 to the ventilation gas mixture. Arterial pCO2 increased within 5 min from a pre-hypercarbic value of 36.4 +/- 6.1 mm Hg to 200-220 mm Hg and was maintained at this level for over 1 hour. Hypercarbia led to rapid cerebral acidification. Intracellular pH decreased from 7.18 +/- 0.08 (pre-hypercarbic period) to 6.68 +/- 0.06 (n = 4) at 10 min and remained stable throughout the NMR observation period. Glutamate decreased to 53 +/- 4% of control after 60 min of hypercarbia, while glutamine increased to 126 +/- 7% of control. Acute hyperammonemia was produced by a programmed intravenous infusion of 250 mM ammonium acetate, which rapidly raised and maintained the concentration of ammonium ions in the blood at approximately 500 microM. Shortly after the start of the infusion (10-20 min), the levels of glutamine and lactate rose continuously throughout the experiment, reaching levels of 170 +/- 25% and 260 +/- 60% of control, respectively (n = 12) after 50 min. Glutamate decreased during the same time interval to 80 +/- 4% of control (n = 12).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral metabolic studies in vivo by combined 1H/31P and 1H/13C NMR spectroscopic methods. 842 59

Noninvasive mechanical ventilation (NMV) now represents the first step in the management of acute on chronic respiratory failure (A/CRF). During the last 5 yrs, many studies have confirmed the feasibility of NMV in an acute setting, either by facial or nasal interface, used in addition to volumetric or barometric respirators, to manage A/CRF. The best indications for NMV are slowly progressive A/CRF, frequently represented by chronic obstructive pulmonary disease (COPD), or restrictive pulmonary disease. The criteria to initiate NMV in such patients are worsening of respiratory status and arterial blood gas (ABG) values, with increased hypoxia, hypercapnia and respiratory acidosis, despite optimal management with medication, physiotherapy and oxygen therapy. Respiratory encephalopathy is not an absolute contraindication; however, bronchial hypersecretion indicates that care is needed under NMV. Invasive mechanical ventilation with endotracheal (ET) intubation is discussed in the case of failure of NMV, when clinical status and ABG values worsen in spite of it. The signal for ET intubation is then obvious, represented by severe dyspnoea leading to respiratory pauses or arrest, severe cyanosis, and signs of haemodynamic instability. Despite immediate evidence of ominous cardiorespiratory inefficiency, ET intubation may be delayed and often avoided with the help of NMV. Criteria should be studied to identify guidelines for cessation of NMV, in order not to continue with the technique too long considering the safety of the patient. Indications for NMV in other kinds of ARF have received less study and are more controversial.
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PMID:Noninvasive mechanical ventilation and acute respiratory failure: indications and limitations. 915 23

Respiratory insufficiency appearing during chronic lung diseases leads to hypoxemia, hypercapnia, acidosis, right ventricular failure and secondary polyglobulia. These disturbances lead to respiratory encephalopathy which is characterized by the appearance of various types of neurological syndromes. We present here the case of a patient suffering from chronic spastic bronchitis accompanied by pulmonary emphysema, whose consciousness disturbances, a generalized epileptic seizure and hemiparesis were connected with his respiratory insufficiency intensifying during the basic disease. Removal of metabolic disturbances caused by respiratory insufficiency has a key role in preventing secondary neurological syndromes.
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PMID:[A case of hypoxic encephalopathy in the course of chronic spastic bronchitis and pulmonary emphysema]. 1110 77

Permanent tracheotomy was the first surgical procedure proposed for the treatment of severe obstructive sleep apnoea syndrome and is still the only surgical option that ensures, even in very severe cases, complete elimination of apnoea and, in turn, clinical remission. Improved knowledge of the causes of obstructive sleep apnoea syndromes and the increasing therapeutic options (instrumental, medical and surgical) have resulted in cases requiring tracheotomy as the only indispensable therapeutic option becoming more rare. At present, the only indications are in very occasional conditions of life-threatening obstructive sleep apnoea syndromes and in patients on whom continuous positive airway pressure is not tolerated or is not effective (severe deoxygenation or hypercapnia, severe respiratory disorder index, severe obstructive sleep apnoea syndrome-related arrhythmias, severe excessive daytime sleepiness, heart diseases or ischaemic encephalopathy exacerbated by obstructive sleep apnoea syndromes, obstructive pneumopathy exacerbated by obstructive sleep apnoea syndromes, severe obstructive sleep apnoea syndromes with few chances of resolution with other surgical procedures or failure of the latter). Moreover, it is the only therapeutic solution in rare nocturnal laryngeal stridor due to multisystemic atrophy (in which obstructive sleep apnoea syndrome is due to nocturnal laryngospasm of neurologic origin). Therapeutic tracheotomy must be permanent (tracheostomy) and, therefore, preferably carried out with a specific technique (skin-lined tracheotomy), able to guarantee greater stability, less risk of granulation tissue, wider opening of the tracheostomy, sufficient reversibility. In our experience, very few patients (10 cases) withsleep disorder breathing have been submitted to skin-lined tracheotomy. Of these, the majority were submitted to surgery for severe apnoea due to nocturnal laryngospasm on account of multisystemic atrophy (n = 7), while only 3 cases of obstructive sleep apnoea syndromes were submitted to skin-lined tracheotomy, i.e., 0.7% of the 424 patients operated on for obstructive sleep apnoea syndrome and 1.7% of the 175 operated on for severe, or very severe, obstructive sleep apnoea syndromes (RDI > 40). Skin-lined tracheotomy was not followed by important complications and expected results were achieved with immediate disappearance of daytime symptoms and considerable improvement in nocturnal apnoea. Besides sleep-related disorders, numerous clinical situations with indications for a permanent tracheotomy may benefit from the skinlined technique, such as severe laryngeal or tracheal stenoses, laryngeal diplegias, miasthenia gravis, lateral amyotrophic sclerosis, intractable aspiration, severe emphysema.
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PMID:Role of skin-lined tracheotomy in obstructive sleep apnoea syndrome: personal experience. 1546 94

We report the first case of witnessed sudden death of an Emery-Dreifuss muscular dystrophy (EDMD) patient with a properly functioning implantable cardioverter-defibrillator (ICD). This 38-yr-old woman with normal left ventricular function had a history of recurrent syncope and nonsustained ventricular tachycardia, for which a single-chamber ventricular ICD was implanted. She later collapsed suddenly and unexpectedly while at home, with witnesses present, and was found cyanotic with pulseless electrical activity by the emergency squad. This event took place in the setting of previously documented hypercapnic ventilatory insufficiency, for which she had refused the use of respiratory muscle aids to normalize alveolar ventilation. Subsequent interrogation of the ICD demonstrated normal function, with no evidence of ventricular tachycardia or ventricular fibrillation. In the hospital, her myocardial function was found to be normal by echocardiography. Further workup revealed that the patient had severe anoxic encephalopathy. She was eventually made "do not resuscitate," and she died on the sixth day of hospitalization. An autopsy was performed, and no obvious cause for the sudden death could be established. Review of the clinical presentation, with all the data available, suggests acute respiratory failure as the likely primary cause of this patient's sudden death, which then secondarily led to the observed pulseless electrical activity of the heart. The use of respiratory muscle aids--in particular, noninvasive mechanical ventilation to prevent chronic hypercapnia and cor pulmonale--is crucial for EDMD patients with symptomatic ventilatory insufficiency, for whom sudden deaths may not necessarily be of primarily cardiac origin.
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PMID:Sudden death in an Emery-Dreifuss muscular dystrophy patient with an implantable defibrillator. 1835 23


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