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

A series of 34 cases of SCUBA-related fatalities in military personnel from the files of the Armed Forces Institute of Pathology has been presented. It may be concluded that the potential problems that can occur in the hyperbaric aquatic milieu while using scuba are not completely appreciated by pathologists. The resulting investigations of such fatalities give little hard data relevant to such entities as true incidence of barotraumatic injuries, aseptic bone necrosis, and contaminated air supply, the interrelationship of human, environmental, and life support system factors in such fatalities, and the pathophysiologic sequences leading to drowning or death due to causes other than drowning. Hyperbaric pathophysiology is reviewed with the hope that more reasonable interpretations of cause and mechanisms of death will be possible, and the entities air embolism and decompression sickness are differentiated in a similar light. The importance of the type of SCUBA is discussed, through analysis of ten operational diving fatalities, and the possibility of anoxia, hyperoxic convulsions, and hypercapnia existing with the use of rebreather SCUBA is emphasized. A general approach to the medical investigation of a SCUBA fatality is given, under broad headings including on-the-scene investigation, clothing and equipment examination, external and internal examinations, and toxicologic examination.
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PMID:Scuba diving deaths: a review and approach for the pathologist. 86 16

1. The breathing pattern, that is the relation between tidal volume (VT) and the inspiratory (TI) and expiratory (TE) durations, has been studied for individual breaths (forty in each steady state). 2. Five healthy subjects were studied in steady-state exercise on a bicycle ergometer breathing air; three of them were also studied in hypercapnia, at rest and during exercise, and two of them also during exercise on a treadmill. 3. Tidal volume and respiratory frequency both increased with work load. The increase in frequency was largely due to a progressive decrease in TE; TI also decreased. 4. At any constant level of respiratory drive (constant work load or chemical load) VT was positively correlated with both TI and TE in more than 95% of cases. 5. A simple model of the respiratory cycle which fits both the observed mean and breath-by-breath patterns and which involves no new assumptions is presented.
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PMID:Mean and breath-by-breath pattern of breathing in man during steady-state exercise. 118 79

Local anaesthetics are responsible for 5 to 10% of all reported adverse reactions to anaesthetic drugs. Adverse effects may be classified as: (a) those associated directly with blocking ion channels in cell membranes, such as cardiovascular and CNS toxicity; (b) those due to other effects of drug or vehicle (mainly peripheral nerve complications); (c) allergic reactions (often a mistaken diagnosis); and (d) mechanical or other effects of technique, such as needle trauma or introduction of infection. Signs and symptoms of CNS toxicity include convulsions, followed by coma and respiratory depression. Convulsions are due to disinhibition of nervous conduction, probably by an action at the gamma-aminobutyric acid (GABA) receptor complex, while depressant effects, which predominate at higher doses, are due to blockade of sodium channels. CNS toxicity is potentiated by hypoxia and hypercapnia, so acute management must minimise these. Cardiovascular toxicity also involves sodium channel blockade, reducing contractility and interfering with conduction. Bupivacaine differs from lidocaine (lignocaine) in the sudden occurrence of dangerous ventricular arrhythmias including fibrillation at subconvulsant doses. Ropivacaine is a newer amide local anaesthetic with toxicity intermediate between these but potency similar to bupivacaine. Neurotoxic complications leading to prolonged deficit after intraspinal administration are uncommon. Causes are multifactorial, and include pH of and additives to preparations. Allergic reactions account for only 1% of untoward reactions, but anaphylactoid collapse can be lifeth-reatening and requires rapid and effective management.
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PMID:Adverse effects of local anaesthetics. 150 66

1. The respiratory effects of corticotrophin-releasing factor (CRF) and the CRF antagonists alpha-helical CRF 9-41 (alpha hCRF) and [DPhe 12, Nle 21-38] rCRF (12-41) (DPhe CRF) have been studied in unanaesthetized fetal lambs of 125-140 days gestation. 2. CRF when given as a 10 micrograms bolus followed by a 5 micrograms h-1 infusion into a lateral cerebral ventricle caused prolonged continuous fetal breathing movements which were stimulated in both amplitude and frequency but which did not persist during hypoxia. 3. Lower doses of CRF (20 ng bolus followed by 10 ng h-1) increased the amplitude but not the frequency of fetal breathing movements which did not become continuous. 4. At higher doses (20 micrograms bolus followed by 10-15 micrograms h-1) CRF induced cerebral convulsions which were also associated with fetal breathing movements of increased amplitude and frequency. 5. The CRF antagonists alpha hCRF and DPhe CRF both inhibited fetal breathing movements and induced a prolonged apnoea which was resistant to the stimulatory effects of 5-6% hypercapnia. 6. We conclude that CRF stimulates breathing movements in the fetal lamb. The finding that administration of the CRF antagonists alone cause apnoea suggests that CRF may have a tonic role in the regulation of fetal breathing movements.
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PMID:The effects of corticotrophin-releasing factor and two antagonists on breathing movements in fetal sheep. 234 87

During the winter of 1986-1987, 64 children with respiratory syncytial virus (RSV) infection were admitted to our hospital. The diagnosis was made by direct immunofluorescent antibody technique. Twenty-three children (36%) needed intensive care treatment. Nearly 11 (52%) had a preexisting disease state, identified as a risk factor i.e., prematurity (n = 8), bronchopulmonary dysplasia (n = 2), congenital heart disease (n = 1). Twelve patients (50%) were intubated and ventilated. Conditions for intubation and ventilation were repetitive apnea with or without bradycardia (n = 4), clinical deterioration (n = 3) or hypercarbia (n = 5). Seventy-five percent of the patients who needed intensive care management were under three months of age compared to 34% of the children who were admitted to the clinical ward. The mean age for ventilated patients was 7.9 weeks. The mean duration of ventilation was 5.5 days. Volume controlled ventilation was initially applied to all patients. Pulmonary complications (atelectasis, pneumonia, pneumothorax or adult respiratory distress syndrome) were present in 15 (65%) IC patients. Nine (39%) of them also had symptoms of inappropriate antidiuretic hormone secretion (IADHS). Only two patients had symptoms of IADHS and two others had convulsions. Three children (5%) died as a result of respiratory insufficiency. Two of these infants belonged to the risk group.
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PMID:Respiratory syncytial virus infections in children admitted to the intensive care unit. 281 76

Local anaesthetic systemic toxicity is a rare but often dramatic complication of regional anaesthesia. Convulsions often follow warning signs, easily recognized when looked for; but they may occur from the first. They are rapidly followed by hypoxia and hypercapnia which greatly enhance the risk of severe cardiac depression, mainly with bupivacaine or etidocaine. Thiopentone is able to stop convulsions quickly, but may further depress the cardiovascular system. Diazepam has been shown to be effective in the treatment of local anaesthetic-induced convulsions. It gives less myocardial depression, but is much slower in effect. Midazolam, a new short-acting benzodiazepine, should be the best choice. Should tracheal intubation become necessary, suxamethonium can be used. Indeed, the principal use of these drugs is to make ventilation easier, so as to restore rapidly correct oxygenation. Severe cardiac depression, often leading to cardiac arrest, may occur from the first or after the appearance of convulsions. It generally follows a regional block carried out with bupivacaine. A few antiarrhythmic drugs have been used to treat ventricular arrhythmias, either in experimental studies (lidocaine, bretylium) or after clinical accidents (lidocaine). Their efficacy and innocuity have to be proved before they can be proposed to treat these accidents. Bradycardia only needs treatment with atropine when it causes severe haemodynamic disturbances. When cardiac arrest occurs, cardiopulmonary resuscitation must be carried out; its mainstays are: oxygen, sodium bicarbonate, adrenaline, calcium and perhaps glucagon. This must be continued for a long time, as late successes have been published.
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PMID:[How should a toxic accident be treated?]. 290 Jun 15

A model of the respiratory control system incorporating both chemical and respiratory neuromechanical feedbacks is proposed to describe the steady-state ventilatory responses to CO2 inhalation and exercise. It is postulated that ventilatory output (VE) is set by the respiratory center to minimize a net operating cost representing the conflicting challenges of arterial chemical imbalance and respiratory-mechanical discomfort (intolerance of effort), given, respectively, by a quadratic function of arterial PCO2 and a logarithmic function of VE. In addition, the system is assumed to be mechanically limited at maximum VE (Vmax). The predicted responses in VE during moderate hypercapnia, exercise, and ventilatory loading closely mimic those normally observed, even though no separate signal unique to exercise is assumed. As a quantitative validation, the model yielded good fits to ventilatory response data obtained in eight healthy subjects during eucapnic and hypercapnic exercise; the predicted Vmax averaged approximately 77% of the maximum voluntary ventilation in all subjects. The results demonstrate the plausibility of the proposed optimization mechanism and suggest an important role for respiratory-mechanical factors in the control of VE.
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PMID:Ventilatory control in hypercapnia and exercise: optimization hypothesis. 311 8

The effect of generalized seizures on local cerebral blood flow was studied autoradiographically in 21 immature marmoset monkeys, using either [123I]- or [131I]isopropyliodoamphetamine. Generalized convulsions were induced in ketamine-anesthetized and awake monkeys with bicuculline and continued for 4-59 min. During convulsions in marmosets less than 3 weeks of age, there was a striking rearrangement of blood flow in favor of the brainstem pontomedullary region. The ratios of blood flow in pons-medulla to blood flow in cerebral cortex, putamen, ventroposterior thalamic nuclei, lateral geniculate nuclei, cerebellum and hemispheric white matter increased 1 1/2 to 2 times compared to controls. In seizure animals 4-8 weeks of age, the redistribution of blood flow to brainstem did not occur. Although metabolic acidosis developed after 30 min of bicuculline-induced seizures, mean arterial blood pressure, temperature, arterial pO2 and pCO2 did not differ significantly from controls, indicating that hypoxemia, hypercapnia and hypotension cannot explain the altered cerebral blood flow pattern. The redistribution phenomenon could be explained by more pronounced vasodilatation in brainstem than many other brain regions during generalized seizures in newborn monkeys. Lack of significant vasodilatation in forebrain structures such as cerebral cortex could contribute to neuronal damage by limiting substrate supply at a time of increased metabolic activity.
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PMID:Preferential blood flow to brainstem during generalized seizures in the newborn marmoset monkey. 380 66

Awake, unanesthetized, and paralyzed sheep made hypoxic and acidotic were given equivalent low and high intravenous doses of lidocaine and bupivacaine over 10 sec. Within 30 sec of injections, all animals had electroencephalographic evidence of convulsions. After administration of low-dose lidocaine, arrhythmias associated with significant hemodynamic changes did not occur; after administration of high-dose lidocaine, half of the animals became hypotensive but had no arrhythmias other than sinus tachycardia. However, after administration of low-dose bupivacaine, all sheep had evidence of serious electrocardiographic changes or arrhythmias, and one animal died. After administration of high-dose bupivacaine, serious electrocardiographic changes occurred in all animals, and despite resuscitative efforts, all died. The most common abnormality after bupivacaine administration was a wide-QRS-complex bradycardia, occurring in most animals regardless of dose. Two-thirds of the animals given high-dose bupivacaine had electromechanical dissociation and subsequent refractory asystole. Although the mechanism of action is not known, bupivacaine appears to be more cardiotoxic than lidocaine. This toxicity is enhanced in animals by the presence of hypercarbia, acidosis, and hypoxia.
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PMID:Bupivacaine-induced cardiotoxicity in hypoxic and acidotic sheep. 405 Dec 6

Rhythmic activity was observed in over 100 pial vessels in 58 cats with a photometric technique through a cranial window. Diameter oscillations with a frequency of mostly 5/min were present at normal mean arterial pressure (MAP) in about half of the animals. When spontaneous activity was absent the same type of oscillations could be provoked by varying MAP, mostly by lowering it to a level of around 60 mm Hg. If a rhythmic activity was present, it could be abolished by increasing and decreasing MAP. Likewise, rhythmic activity ceased during strong vasodilatation caused by hypercapnia, hypoxia, Ca antagonists or other vasoactive drugs. Rhythmic activity also decreased in amplitude or disappeared with vasoconstriction accompanied by a stable MAP. Rhythmic activity of pial vessels thus seemed to occur within an as yet unspecified range of vessel wall tensions mediated via intraluminal pressure and a state of constriction or dilatation. This rhythmic activity was not primarily influenced by sympathetic stimulation, alpha-sympathetic blockade, hyper- or hypocapnia, hypo- or hyperoxygenation. Moreover, the vascular activity fits well with the description of rhythmic smooth muscle activity in other vascular beds and organs in vitro and in vivo, ascribed to myogenic regulatory processes. Therefore, it is suggested that the rhythmic activity of pial vessels might be an expression of myogenic blood flow regulatory activity in the brain.
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PMID:Rhythmic activity of cat pial vessels in vivo. 611 76


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