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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In case of cranial trauma, early respiratory troubles either of central or peripheral origin often accelerate the deterioration of the neurological situation. The different values of PCO2, PO2, pH and alcaline reserve measured on samples of CSF in comatose patients prove the central acidosis related to metabolic and vascular disorders in the damaged areas. Our results confirm the correlation between the importance of this disturbances and the severity of the trauma. It is thus necessary to insure patients of satisfactory respiration conditions. The tracheobronchial cleansing is applicable to intubated or tracheotomized patients by an instillation of 5ml of simple or bicarbonated physiological serum 4 to 6 times a day, followed by repeated aspirations and associated to a preventive endotracheal instillation of 80 mg of Gentamycin 4 times a day. Moreover we use controlled respiration which does not modify the gazometric parameters in the CSF but which assures patients a normoxia and moderate hypocapnia with a decrease of intracranial hypertension. Treatment by controlled hyperventilation must be precocious, because the recuperation at the level of the damaged zones is very slow.
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PMID:Treatment of comatose patients by mechanical hyperventilation. 0 50

From this analysis we may conclude that the most important factors influencing the outcome of coma due to injury are age, vegetative state, level of coma, decerebration, and hypocapnia. In all cases where a combination of four or more of any of the above-mentioned factors was present the patient died. EEG seems less predictive in the early period, but may give some information for late prognosis.
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PMID:Factors influencing the outcome of coma in severely injured patients. 29 Jan 39

Changes in cerebral blood flow (CBF) and in O2 consumption caused by anaesthetic agents were studied in 36 subjects in coma after cranial trauma. These changes can be divided into 3 groups: (1) Reduction in CBF and in O2 consumption of about the same percentage, after penthiobarbital, gamma-OH and alfathesin. (2) A reduction in CBF greater than in O2 consumption after diazepam and chlorpromazine. (3) Increase in CBF without significant change in O2 consumption after ketamine. The haemodynamic changes occur in the same direction whatever the initial value of the CBF (normal, hypoperfusion or hyperaemia). The reduction in CBF caused by gamma-OH is associated with a decrease in the arterio-venous difference in O2 (DAVO2). Gamma-OH also prevents the increase in DAVO2 observed in hypocapnia provoked by hyperventilation. These properties are an indication for using gamma-OH, alone or associated with hyperventilation, in reactive cerebral hyperaemia. Comparison of the E.E.G., CBF and cerebral O2 consumption shows that the E.E.G. changes produced by anaesthetic agents, such as fast spindles and burst suppression, are not related to any particular haemodynamic or metabolic state. The E.E.G. changes induced by penthiobarbital or diazepam can be corrected, at the same time as changes in CBF and O2 consumption, by injecting doxapram.
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PMID:[Effects of drugs used in anaesthesia and in neurosurgical intensive care on the blood flow and metabolism of the brain (author's transl)]. 90 21

In a five year period, 39 children (29 boys, 10 girls) aged 2 months to 13 years (mean 7.8 years) were studied who had suffered a major head injury (29 road traffic accidents, six falls, and four non-accidental injury). The injury had been assessed clinically and by cranial computed tomography or cranial ultrasound (in a single baby of 2 months). Initial Glasgow coma scores for all subjects ranged from 3-11 (mean 5.5), intact survivors 5-11 (7.4), minor handicap 4-11 (6.1), major handicap 3-6 (4.3), fatalities 3-6 (4.1). All were treated with sedation, paralysis, hyperventilation (arterial carbon dioxide tension 3.0-3.5 kPa), intracranial pressure monitoring and moderate body surface hypothermia to 32 degrees C. Nine children died and 30 survived (nine intact, 13 minor disability, and eight major disability). The worst cerebral perfusion pressure was over 40 mm Hg in all but one survivor, and less than 40 mm Hg in seven of nine fatalities. Severe hypocapnia both in the first 24 hours and overall was correlated with poor outcomes (dead or major disability), as were bilateral contusions or diffuse axonal injury.
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PMID:Management and outcome of severe head injuries in the Trent region 1985-90. 833 80

Manual ventilation is frequently performed by nurses to control increases in intracranial pressure (ICP) or during physiotherapy in head injured comatose patients. The effects of manual ventilation (n = 251) on ICP, cerebral perfusion pressure (CPP) and EEG have been studied in 18 mechanically ventilated patients. A fall in ICP was easily obtained but a fall in arterial blood pressure was often present at the same time. Thus a reduction in CPP resulted in 36% of occasions. Prophylactic boluses of thiopental (n = 67) before noxious stimuli obtained a fall in ICP in 99% of occasions but resulted in a decrease in CPP in 46%. The fall in ICP, due to the decrease in cerebral blood flow (CBF) by hypocapnia or metabolic depression and/or arterial hypotension, may be beneficial in hyperaemic brains but may precipitate cerebral hypoxia in ischaemic lesions. Relevant information about cortical metabolism (CMR) may be obtained from EEG monitoring by Cerebral Function Monitor but, unfortunately, no data about CBF are clinically available. The Authors suggest that the continuous monitoring of jugular bulb oxygen saturation (SjO2) may offer a clinically useful index of CBF adequacy to CMR. Findings from a preliminary study in 5 patients demonstrate that a severe decrease in SjO2 has been frequently caused by manual ventilation, hypothetically related to severe cerebral ischemia. High levels of SjO2 have been induced by endotracheal suction and physiotherapy, probably related to severe hyperemia. As prevention of ischaemic and hyperaemic insults is a major goal of treatment, the A. suggest that these undesirable effects of nursing might be avoided if nurses could take advantage of continuous monitoring of SjO2.
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PMID:[Continuous monitoring of O2 saturation in cerebral blood. A guide for the nursing of brain trauma patients in coma]. 162 Apr 53

A new index of cerebral hemodynamics, cerebral hemodynamic reserve (CHR), was evaluated in 12 comatose adults with severe, acute, traumatic, diffuse swelling of the brain, who underwent continuous monitoring with a fiberoptic catheter of the saturation difference in arteriojugular oxyhemoglobin. CHR was assessed as the ratio of changes in global cerebral oxygen extraction to changes in cerebral perfusion pressure (CPP) as a result of spontaneous increases in intracranial pressure (ICP). During the course of hyperventilation (Pco2 in the range of 20 mm Hg) for ICP control below 20 mm Hg, 34 observations were made over the initial 48 hours postinjury. Despite normal CPP, in 25 of the observations (73.5%), ICP elevations to the range of 20 mm Hg were associated with compromised CHR, as evidenced by decreases in jugular oxygenation directly attributed to the ICP increases. In the remaining nine observations (26.5%), CHR was preserved, as evidenced by no changes or increases in jugular oxygenation when ICP increased. The CHR improved on the second day, suggesting an improved tolerance of the cerebral hemodynamics to ICP increases. Before the ICP elevations, in most of the observations, the global cerebral blood flow was estimated as being optimally decreased (by hypocapnia), in relation to cerebral oxygen consumption. This was reflected by the occurrence of baseline normalized cerebral oxygen extraction. It is concluded that in this group of patients, under circumstances of profound hyperventilation, ICP elevations within the normal CPP range may result in decreased cerebral oxygenation, even when the normal CPP would imply otherwise. It is suggested that CHR assessment may provide information regarding the status of intracranial "tightness," insofar as cerebral circulation and oxygenation are concerned.
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PMID:Continuous monitoring of cerebral oxygenation in acute brain injury: assessment of cerebral hemodynamic reserve. 196 6

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

A case is reported of a 40-year-old woman presenting with cerebral malaria complicated by an adult respiratory distress syndrome (ARDS). The patient was admitted to the intensive care unit in a coma, scored 5 on the Glasgow scale. Plasmodium falciparum parasitaemia was, at the time, 50%. A continuous intravenous quinine infusion (25 mg.kg-1.day-1) was started, together with the required symptomatic treatment. Blood was transfused because of increasing anaemia (haemoglobin 60 g.l-1). After 24 h, parasitaemia was 12%, consumption of clotting factors broke out (prothrombine 43%, fibrin degradation products greater than 40 micrograms.ml-1, platelets 45 G.l-1). Hypoxaemia (PaO2 = 46 mmHg) and hypocapnia (PaCO2 = 32 mmHg) became obvious, together with bilateral diffuse alveolar infiltrates on chest X-ray. Haemodynamic data suggested non cardiogenic oedema: PEEP 20 cm H2O, cardiac output 6.15 l.min-1, mean pulmonary arterial pressure 35 mmHg, pulmonary wedged pressure 15 mmHg. The hypoxia worsened and the patient died on the 15th day after associated with high levels of parasitaemia. Several reports have suggested that it may be related to increased capillary permeability. Initial fluid overload should therefore be avoided. Parenteral quinine remains the mainstay of treatment, because of its rapid schizonticidal activity. Although exchange transfusion seems to be a valuable adjunct to chemotherapy, it requires further assessment.
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PMID:[Fatal pulmonary edema in a pernicious malaria attack]. 227 23

Twelve patients who were comatose after head injuries were studied with serial determinations of regional cerebral blood flow, jugular PO(2) tension, and intraventricular pressure. These determinations began a few hours after the injury, and were followed throughout the clinical course. Diffuse derangement of cerebral vasomotor regulation is confirmed after severe head trauma, which may contribute to deterioration and poor prognosis, and which indicates a need for therapeutic maintenance of rich oxygenation, hyperventilation with moderate hypocapnia, and steady blood pressure. Continuous recording of IVP (eventually sensitized by fluid infusion or CO(2) inhalation tests) may give an early indication of the subsequent clinical state and may suggest the need to submit the patients to further investigative and therapeutic procedures.
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PMID:Regional cerebral blood flow and intraventricular pressure in acute head injuries. 437 73

Six children who remained in deep coma after immersion accidents in fresh water received therapy to maintain normal intracranial pressure (ICP). This involved controlled ventilation to ensure hypocapnia and hyperoxaemia, maintenance of low normothermia, fluid restriction, dexamethasone (1-1.5 mg/kg initially, 1-1.5 mg/kg/day as maintenance) and barbiturates (phenobarbitone and thiopentone). The latter were given in a wide range of dosage. Increased ICP was common to all patients, but could always be kept at acceptable levels. All patients suffered from pulmonary oedema; three developed broncho-pneumonia and two developed adult respiratory distress syndrome. All children survived with good recovery, two needed active rehabilitation for several months.
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PMID:Intensive care after fresh water immersion accidents in children. 718 Oct 62


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