Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypocapnia during extracorporeal circulation in hypothermia increases oxygen consumption. Po2 in mixed venous blood decreases. This probably reflects a decrease in tissue oxygen tension. Hyperventilation will therefore increase the risk of hypoxia in critically perfused tissues. Therefore we recommend to keep PaCO2 (T) constant at 40 mm Hg during hypothermia.
 ...
PMID:[The influence of PaCO2 on oxygen consumption during extracorporeal circulation in hypothermia (author's transl)]. 0 89

Pulmonary complications after cardiac surgery under extracorporeal circulation remain frequent and sometimes grave, in spite of the great progress which has been made over the past 20 years in the methods of cardiorespiratory assistance. The authors analyse the clinical and radiological repercussions of perfusion on the lung, in 40 patients operated under ECC for coronary revascularisation. The simutaneous study of the arterial, and mixed venous blood gasses and of the alveolar gases, in 20 of these patients showed the constant occurrence of a shunt syndrome, without alveolar hypoventilation or disorders in peripheral circulatory flow. Ventilatory alcalosis, hypocapnia, hypoxemia and the rise in the alveolar arterial oxygen gradient is increased during the second post-operative day. Among the variables studied (duration of ECC, degree of hypothermia, duration of the intervention, duration of anesthesia, pleurotomy) only the latter intervened in a statistically significant manner in this study, in the increase in hypoxemia. 46 pulmonary biopsies carried out before and after ECC in 23 coronary patients were examined with the electron microscope. The initial alveolar involvement affects the septal microcirculation with signs of an increase in capillary permeability leading to an interstitial and epithelial destruction. The use of a membrane oxygenator prevents some of the alveolar lesions, as has been proved by the study of five pulmonary biopsies carried out in dogs submitted to ECC of long duration. Catherterization of the pulmonary artery carried out in 35 patients by means of a SWAN-GANZ catheter, before the intervention enabled supervision of the degree of importance and speed of the hemodynamic variations in the pulmonary circulation during the different phases of ECC (during the phase of ventricular fibrillation). The rise in the flow of left output can lead to the occurrence of negative pulmonary intravascular pressures which can be prejudicial for capillary trophicity. The syndrome of "ECC lung", a veritable "induced post-agressive lung" must be placed in the group of refractory hypoxemia of which it represents one of the most typical pictures.
 ...
PMID:[Pulmonary complications after extracorporeal circulation. ECC lung syndrome]. 1 38

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
 ...
PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

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.
 ...
PMID:Management and outcome of severe head injuries in the Trent region 1985-90. 833 80

1. Two hours of exposure to heat stress, resulted in hyperthermia in rabbits (Oryctolagus cuniculus). 2. This was accompanied by a severe hypocapnia, partly compensated for by a significant decrease in bicarbonate (HCO3-) concentration. 3. The severest hyperthermia (Tb = 43.5 degrees) was followed by a sharp decreased in both PaCO2 (to 20.2 torr) and HCO3- (to 9.2 mM/l), resulting in extreme metabolic acidosis (pH = 7.290). 4. The significant increase in serum osmolality (27%) is interpreted by the cumulative effect of increased electrolyte and metabolite concentrations. 5. The elevation in blood BUN, creatinine, globulin and GOT levels point to a possible damage to muscle cells by hypothermia. 6. The stable cholesterol and alkaline phosphatase levels, suggest that liver tissue was not damaged. 7. The dramatic increase in glucose from 103.8 to 348.8 mg%, and the significant increase (from 22.0 to 39.9 mg%) in BUN, suggest a possible disability of the cells to metabolize carbohydrates, accompanied by a progressive proteolysis as an alternative process for energy production. 8. The data suggest that the emergence of muscle cell damage, severe hyperglycemia and acidosis under heat stress, precedes and amplifies the deteriorating effects of high Tb in heat stressed rabbits, which often lead to mortality.
 ...
PMID:The effect of heat exposure on blood chemistry of the hyperthermic rabbit. 198 37

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
 ...
PMID:Myocardial protection: what the anesthesiologist does. 213 51

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.
 ...
PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

A 31-year old primigravida was admitted at 31 week gestation for subarachnoid haemorrhage. Cerebral angiography revealed an aneurysm on the left middle cerebral artery. Eleven days later, the aneurysm was clipped off. General anaesthesia was induced with thiopentone, pancuronium and fentanyl, and maintained with fentanyl (40 micrograms.kg-1) and isoflurane in air/O2 with a non-rebreathing circuit. The patient was mechanically ventilated to maintain mild hypocapnia. Arterial hypotension was induced by increasing the inspired isoflurane concentration from 1 to 3 vol%. The response was immediate and a mean arterial pressure of 60 mmHg was maintained for 80 min with an inspired isoflurane concentration of 2.5 vol%. Foetal heart rate was monitored before, during and after general anaesthesia. Loss of beat to beat variation was observed after induction, and foetal heart rate slowly decreased from 150 to 115 b.min-1 at the end of the operation. Postoperative state was good, except for transitory aphasia. At 35 week gestation, the patient went into premature labour, with hypothermia of 39.5 degrees C; an emergency caesarean section was performed. The 2,340 g female infant had a 10 min Apgar score of 8. One month later, clinical examination of the mother and daughter was quite normal. The precautions and anaesthetic management of patients suffering from ruptured cerebral aneurysm during the end of pregnancy are reviewed. Hypotensive agents are discussed.
 ...
PMID:[Hypotension induced by isoflurane for the treatment of intracranial aneurysm in late pregnancy]. 343 89

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
 ...
PMID:A study of profound hypothermia by surface cooling. 677 40

Cerebral protection combines techniques aimed 1) to avoid death of neurones which sustained primary ischemic of traumatic insults and 2) to prevent secondary insults to the brain. The chemical brain retractor concept includes the use of a total intravenous anesthesia technique, mild hypocapnia and mannitol with strict monitoring and maintenance of the global cerebral homeostasis. This contributes to decrease brain volume and intracranial pressure and allows the best possible access to the operating site, while avoiding excessive pressure under the surgical brain retractors. Neuronal protection is based on a better understanding of the biological basis of secondary brain damage; therapeutic or prophylactic techniques include the use of specific pharmacological agents, hypothermia, hemodilution and maintenance of an elevated cerebral perfusion pressure. In short, although the favourable effects of such techniques are nor easy to demonstrate in man, their use in today's clinical practice, in association with the concept of the chemical brain retractor, is an effective way to prevent ischemic cerebral insults during neurosurgical procedures.
 ...
PMID:[Relaxation and protection of the brain on the operating table]. 759 56


1 2 3 Next >>