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

The authors report the values of mean hemispheric blood-flow and cerebral arterial consumption they found in 34 neurosurgical comatous cases in acute state. In basal conditions, mean values of mean hemispheric bloodflow and oxygen consumption are lowered. There seems to be a relation between the values found and the comatous stage on one hand, the prognosis on the other hand. The cerebral response to hypercapnia (16 assays) allows to separate 2 groups, one with a noticeable improvement of cerebral bloodflow, the other with only a minimal response. There was no significant variation of cerebral oxygen consumption in both group. Cerebral response to CO2 seems to be clearly related to the stage of coma (low in the most severe cases) but pronostic incidence remained uncertain. A hypertensive test by means of Aramine (18 assays) allows to separate 3 groups : 1 group (8 cases) where the mean hemispheric bloodflow remained stable during hypertension as did the cerebral oxygen consumption -(autoregulation remained unchanged), 1 group (4 cases) where mean hemispheric bloodflow and cerebral oxygen consumption were lowered (excessive autoregulation), 1 group (6 cases) where mean hemispheric bloodflow increases clearly while under Aramine perfusion (loss of autoregulation). Those dynamic tests, either hypercapnic or hypertensive, allow, in comparing oxygen consumption variations with cerebral bloodflow variations, the distinction between : patients where metabolic autoregulation seems maintained (good prognosis) - (10 cases), patients where metabolic regulation is lost with either "luxury perfusion" (14 cases) - poor prognosis, or "insufficient perfusion" (10 cases). The authors are discussing the treatment concerning those last mentioned patients.
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PMID:[Value of cerebral metabolic exploration in post-traumatic coma states in the acute phase]. 1 86

A 63-year-old man with obstructive pulmonary disease developed severe metablic alkalosis and coma while receiving steroid therapy and nasogastric suction. Treatment, which included the acute induction of hypercarbia and the simultaneous administration of acetazolamide and saline, restored acid-base balance within 24 hours. This combined approach eliminated the need to infuse hydrochloric acid.
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PMID:Life-threatening metabolic alkalosis in a comatose patient. 47 5

In a group of 141 patients treated for coma following poisoning, complications of endotracheal intubation were assessed. The results of this study indicate that prolonged intubation is not quite safe and that serious complications occur in several per cent of cases. Complications are more common when intubation is prolonged over 24 hours. It was observed that hypoxaemia and hypercapnia have an unfavourable effect on the incidence of complications.
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PMID:Complications of endotracheal intubation in patients treated for acute poisoning. 118 Mar 75

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

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

The prehospital treatment of patients with intracerebral hemorrhage must be aimed at prevention of secondary brain damage and provision of an optimal physiologic environment to maximize the potential of recovery. Adequate cerebral oxygenation and the prevention of hypercarbia is a priority. This can only be managed by early intubation and artificial ventilation in patients with a Glasgow-coma-scale below eight, together with the restoration of normal hemodynamics to guarantee adequate cerebral perfusion.
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PMID:[Preclinical management of patients with intracerebral hemorrhage]. 158 80

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

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
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PMID:Human physiology under cold exposure. 181 74

Prior to the start of supportive therapy at the site of the accident, arterial blood samples from 47 patients with acute head injury were taken for blood gas analysis. At the same time, the degree of unconsciousness was assessed using the Glasgow-Coma-Scale. After transport to the hospital, arterial blood gases and the level of unconsciousness were again determined. A very close correlation was found between the initial depth of unconsciousness and the degree of hypercapnia (R = -0.90). Patients with head injury and other multiple injuries did not differ in this report (R = -0.95) from those with isolated head injury. The correlation between PaO2 and the degree of unconsciousness was less well defined, and the results showed a greater degree of scatter (R = 0.54). The acidosis observed resulted mainly from the rise in PaCO2. The absence of any correlation between the base excess and the Glasgow-Coma-Scale levels (R = -0.27) makes a common metabolic derangement unlikely. As a result of intubation and controlled ventilation, the hypercapnia of the comatose patients had been corrected, and a correlation could no longer be found between the Glasgow-Coma-Scale level and the PaCO2. In order to avoid hypoventilation, which carries with it the danger of a rise in intracranial pressure, all patients with severe head injury should be intubated and ventilated as soon as possible after the accident.
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PMID:Arterial blood gases in patients with acute head injury at the accident site and upon hospital admission. 202 64

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41


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