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

Work related head injuries do not occur frequently in comparison to other injuries, but their importance lies in their relative severity, both in terms of work days lost and long term morbidity, making it important for the occupational health nurse to have knowledge of how to deal with the initial injury and residual problems. In head injury, most of the treatment is aimed toward prevention of hypoxia, airway obstruction, hypercapnia, hypotension, and bleeding. The Glasgow Coma Scale is used for the severely head injured person. The residual cognitive impairment, emotional disturbances, and behavioral changes after head injury tend to continue long after the physical disabilities have resolved. Therefore, the occupational health nurse needs to assist recovering individuals and their families and coworkers to learn to cope with physical, cognitive, behavioral, and intellectual deficits.
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PMID:Head injury in the workplace. 222 85

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

CPP reflects perfusion problems related to increased ICP or inadequate MAP. CPP is a most helpful and practical management tool. The relationship of CBF and CPP depends on cerebral vascular resistance (flow equals pressure divided by resistance). At present, we do not have a practical method to measure vascular resistance or CBV. A close relationship between an increase in CBV and increase in ICP exists. However, the relationship between CBF and ICP is more complex. Whereas CBV is strongly dependent on vasodilation and venous return, CBF is influenced by CPP, vascular resistance, viscosity changes, and focally or diffusely increased ICP. For instance, in hypotensive shock one finds a low CBF with an elevated CBV (and ICP) from vasodilation related to hypercapnia, anoxia, or acidosis. Nevertheless, about two thirds of patients with increased ICP after head injury have increased CBF (hyperemia) and increased CBV. This frequent hyperemia is one rationale for the wide usage of hyperventilation to treat increased ICP. It must be recognized that a group of patients may have ischemia caused by excessive hyperventilation therapy for increased ICP. The PaCO2 must not be allowed to decrease to 20 mmHg or lower, but in some patients a PaCO2 level of 21 to 25 may be predisposing to ischemia. Strong consideration is thus given to monitoring CBF and cerebral oxygen metabolism (arteriovenous oxygen content difference [AVDO2], CMRO2) in states of coma and increased ICP. In such patients, continuous infusion of mannitol may result in improved CBF, and hyperventilation therapy can be less aggressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonsurgical management of increased intracranial pressure. 270 May 10

It is known that early mortality after acute craniocerebral trauma (CCT) depends heavily on the extent of any hypoxia and, even more, hypercapnia in the early phase after the trauma. Hypoxia and hypercapnia are very difficult to appraise at the scene of an accident without measuring instruments. It is now generally recognized that appraisal in accordance with the Glasgow coma scale (GCS) is a suitable way of estimating the depth of impairment of consciousness (eye opening in response to stimuli, verbal response to stimuli, motor response to stimuli). The maximum number points is 15, and the minimum, 3. We therefore decided to investigate whether there is a correlation between the degree of impairment of consciousness measured with the GCS and onset of hypercapnia or hypoxia soon after. In 33 patients with acute CCT, arterial blood was taken for analysis of blood gases at the scene of the accident before therapy was started. At the same time, we evaluated the level of consciousness on the basis of the GCS. The blood samples were taken within 6-21 min after the trauma in all patients. It was shown that there is a very close correlation between the severity of trauma (measured with the GCS) and the degree of hypercapnia (r = -0.88). This was true of all CCT patients with multiple trauma without exception. The PaO2 correlates with the severity of trauma (r = 0.60) far less closely, and above all much less consistently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Behavior of blood gases in patients with craniocerebral trauma at the accident site and at the time of admission to the clinic]. 312 Jun 17

Blood gas and haemodynamic changes caused by chronic respiratory insufficiency affect the right ventricle and produce chronic cor pulmonale. Equally important but less well known modifications affect the left ventricle and the general circulation and are the subject of the present report. Hypoxemia, hypercapnia and acidosis caused by severe hypoxia create functional disturbances in both ventricles that are manifested in a volume overload that added to other major malfunctions provoke congestive heart failure. The coronary circulation is affected by metabolic factors, perfusion alterations, right ventricular hypertrophy and concomitant coronary lesions. Advanced respiratory insufficiency caused by poorly compensated respiratory acidosis and metabolic acidosis reduces cardiac output and frequency so that tissue perfusion is compromised. Furthermore alterations in transmembrane electrolytic concentrations produce repeated multifocal ventricular arrhythmias that expose the patient to the risk of sudden death. Cardiac failure is reflected in other organs like the kidney and the central nervous system and also contributes to tissue and cerebral hypoxia. The later depresses the respiratory centres and develops into often irreversible coma. A better knowledge of these elements may contribute to the development of appropriate treatment.
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PMID:[General cardiocirculatory effects in chronic respiratory insufficiency]. 354 42

In three consecutive patients suffering from life-threatening asthma in a comatose state (mean age: 37 +/- 4 yr; Glasgow coma score: 3; bilateral mydriasis), intracranial pressure was monitored with an extradural transducer set-up a mean of 2 h after the onset of the coma. The aims were to detect intracranial hypertension and to improve its therapy. Basal therapy associated: 1) mechanical ventilation; 2) theophylline 1.5 g X 24 h-1, salbutamol 30 mg X 24 h-1, hydrocortisone 2 g X 24 h-1, pancuronium 0.5 mg X kg-1 X 24 h-1; 3) pentobarbitone 35 mg X kg-1 X 24 h-1, normal hydration, normothermia and 30 degrees head-up tilt. If the intracranial pressure rose above 15 mmHg, an i.v. bolus of pentobarbitone (5 mg X kg-1) was given if the barbiturate blood level was equal or below 100 micrograms X l-1. In case of failure, a dose of mannitol (20 mg) completed the therapy if blood therapy was equal or below 320 mosm X l-1. All patients developed intracranial hypertension (21, 53 and 23 mmHg, respectively). The intracranial hypertension followed the bronchospasm and disappeared with it. Hypoxaemia, hypercapnia and high peak airway pressures could explain the intracranial hypertension. All patients recovered without sequelae. This data should make us use with great care all treatments likely to increase the intracranial pressure during life-threatening asthma.
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PMID:[Intracranial hypertension during status asthmaticus]. 357 44

A 25-year-old patient received general anaesthesia for an emergency Caesarean section. Arterial blood gases obtained because of prolonged postoperative coma demonstrated profound hypercapnia (PaCO2 246 mmHg). Examination of the anaesthetic machine revealed a complete disconnection of the metal components of the main gas line downstream from the vaporizer, in a location that was obscured from the anaesthetist's view. Causes of profound hypercapnia are reviewed and preventive measures are discussed.
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PMID:Profound hypercapnia due to disconnection within an anaesthetic machine. 367 89

In metabolic alkalosis, a compensatory decrease in alveolar ventilation with hypercapnia has been noted only rarely. We recently managed a patient with gastric outlet obstruction from a duodenal ulcer who survived after arriving in the emergency room comatose with severe hypochloremic metabolic alkalosis, compensatory hypoventilation, and hypercapnia. We know of no report in the English literature of a patient with gastric outlet obstruction having a respiratory acidosis or hypochloremia as severe as that in our patient. Proper understanding of the pathophysiology of primary metabolic alkalosis due to gastric losses is necessary to correct the acid-base abnormalities quickly and to restore normal alveolar ventilation.
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PMID:Marked hypochloremic metabolic alkalosis with severe compensatory hypoventilation. 376 30

Neurologic injury is a significant source of morbidity and mortality in pediatric patients. In order to clarify the factors influencing outcome in pediatric patients with severe head injury, we studied 200 consecutive patients with Glasgow Coma Scale (GCS) scores of 8 or less. The following data were collected: age, GCS score, presence of mass lesions, oculovestibular reflexes (OVR), pupillary size and reactivity, intracranial pressure (ICP), apnea, presence of hypotension, hypoxia (PO2 less than 60 torr), or hypercarbia (PCO2 greater than or equal to 35 torr), presence of multiple trauma, and Modified Injury Severity Scale (MISS) score. Outcome was assessed by the Glasgow Outcome Scale at a minimum of six months following recovery. Of the 200 patients in the study, 86 (43%) had isolated head injury (IHI) and 114 (57%) had head injury plus multiple trauma (HI + MT). Overall, 26% of patients had mass lesions; 28% had altered OVR; 33% had fixed, dilated pupils; 79% had increased intracranial pressure; and 29% had hypotension, hypoxia, or hypercarbia. Overall mortality was 21.5%. Severity of injury (as judged by presence of mass lesions, GCS, OVR, fixed pupils) was more pronounced in patients with IHI, although increased ICP was more common in patients with HI + MT; however, death was almost three times more common in patients with HI + MT (30% versus 10.5%). In the IHI group, two of nine patients who died (22%) had hypotension, hypoxia, or hypercarbia; all but four patients (88%) in the HI + MT group had hypotension, hypoxia, or hypercarbia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pediatric head injury: the critical role of the emergency physician. 406 90

Fifteen cases of delayed traumatic intracerebral hematoma (DTICH) operatively treated are reported. Patients who are awake or only drowsy on admission (Coma Grades 1 and 2, Grady scale) often undergo dramatic sudden neurological deterioration 48 to 72 hours after admission. Emergency computed tomographic scanning and prompt craniotomy for hematoma evacuation yield excellent clinical results in the majority of cases. Patients presenting in deeper grades of coma (Grades 3 to 5, Grady scale) who develop DTICH do quite poorly, often because the diagnosis is difficult to make and consequently is delayed. The development of DTICH is in our experience highly unpredictable, and often no clear secondary cause (hypercapnia, hypoxia, bleeding diathesis) can be demonstrated.
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PMID:Delayed traumatic intracerebral hematoma: report of 15 cases operatively treated. 669 89


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