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

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.
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PMID:[Hypotension induced by isoflurane for the treatment of intracranial aneurysm in late pregnancy]. 343 89

The perioperative complications associated with cerebral aneurysm surgery require a specific anaesthetic management. Four major perioperative accidents are discussed in this review. The anaesthetic and surgical management in case of rebleeding subsequent to the re-rupture of the aneurysm is mainly prophylactic. It includes haemodynamic stability assurance, maintenance of mean arterial pressure (MAP) between 80-90 mmHg during stimulation of the patient such as endotracheal intubation, application of the skull-pin head-holder, incision, and craniotomy. The aneurysmal transmural pressure should be adequately maintained by avoiding an aggressive decrease of intracranial pressure. Once the skull is open, the brain must be kept slack in order to decrease pressure under the retractors and avoid the risks of stretching and tearing of the adjacent vessels. If, despite these precautions, the aneurysm ruptures again. MAP should be decreased to 60 mmHg and the brain rendered more slack, in order to allow direct clipping of the aneurysm, or temporary clipping of the adjacent vessels. The optimal agents in this situation are isoflurane (which decreases CMRO2), intravenous anaesthetic agents (inspite their negative inotropic effect, they may potentially protect the brain) and sodium nitroprusside. Vasospasm occurs usually between the 3rd and the 7th day after subarachnoid haemorrhage. It may be seen peroperatively. The optimal treatment, as well as prophylaxis, is moderate controlled hypertension (MAP > 100 mmHg), associated with hypervolaemia and haemodilution, the so-called triple H therapy, with strict control of the filling pressures. Other beneficial therapies are calcium antagonists (nimodipine and nicardipine), the removal of the blood accumulated around the brain and in the cisternae, and possibly local administration of papaverine. Abrupt MAP increases are controlled in order to maintain adequate aneurysmal transmural pressure. Beta-blockers, local anaesthetics administered locally or intravenously, a carefully titrated level of anaesthesia, a maintained volaemia play a protective role. Cerebral oedema is sometimes already present at the opening of the skull or may arise later, due to a high pressure under the retractors, to the surgical manipulations of the brain or to brain ischaemia subsequent to temporary clipping. Its treatment is aggressive, with intravenous agents, mannitol, deep hypocapnia and/or lumbar drainage. Prophylaxis, according to the "brain homeostasis concept", is the preferred method to avoid these four peroperative accidents. It includes normal blood volume, normoglycaemia, moderate hypocapnia, normotension, soft manipulation of the brain and optimal brain relaxation.
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PMID:[Peroperative risks in cerebral aneurysm surgery]. 875 91

The purpose of this study was to determine if baseline oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in brain tissue adjacent to an arteriovenous malformation (AVM) is different from measures in control patients. In addition, PO2, PCO2, and pH changes were measured during the course of AVM resection. Two groups were studied. Group 1 (n = 8) were non-ischemic patients scheduled for cerebral aneurysm clipping. Group 2 (n = 13) were patients undergoing neurosurgery for AVM resection. Following craniotomy, the dura was retracted and a PO2, PCO2, pH sensor inserted into non-ischemic brain tissue in Group 1. In Group 2, the sensor was inserted into tissue adjacent to the AVM. Following equilibration, tissue gases and pH were measured during steady state anesthetic conditions in Group 1 and during AVM resection in Group 2. The results show that under baseline conditions before the start of surgery, tissue PO2 was decreased in AVM compared to control patients but PCO2 and pH were not changed. During AVM resection, PO2 increased, PCO2 decreased, and pH increased compared to baseline measures. These parameters did not change in control patients over a similar time period. The results suggest that chronic cerebrovascular adaptation occur in AVM patients with decreased tissue perfusion pressure as an adjustment for decreased oxygen delivery. During AVM resection, this adaptation produces a hyperemic environment with relative tissue hyperoxia, hypocapnia, and alkalosis which is not corrected by the end of surgery.
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PMID:Increased brain tissue oxygenation during arteriovenous malformation resection. 1023 2

You are the attending intensivist in a neurointensive care unit caring for a woman five days post-rupture of a cerebral aneurysm (World Federation of Neurological Surgeons Grade 4 and Fisher Grade 3). She is intubated for airway protection and mild hypoxemia related to an aspiration event at the time of aneurysm rupture, but is breathing spontaneously on the ventilator. Your patient is spontaneously hyperventilating with high tidal volumes despite minimal support and has developed significant hypocapnia. She has not yet developed the acute respiratory distress syndrome. You debate whether to tightly control her partial pressure of arterial carbon dioxide, weighing the known risks of acute hypocapnia in other forms of brain injury against the potential loss of clinical neuromonitoring associated with deep sedation and neuromuscular blockade in this patient who is at high risk of delayed ischemia from vasospasm. You are also aware of the potential implications of tidal volume control if this patient were to develop the acute respiratory distress syndrome and the effect of permissive hypercapnia on her intracranial pressure. In this paper we provide a detailed and balanced examination of the issues pertaining to this clinical scenario, including suggestions for clinical management of ventilation, sedation and neuromonitoring. Until more definitive clinical trial evidence is available to guide practice, clinicians are forced to carefully weigh the potential benefits of tight carbon dioxide control against the potential risks in each individual patient based on the clinical issues at hand.
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PMID:Pro/con debate: should PaCO2 be tightly controlled in all patients with acute brain injuries? 2336 May 55