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

A retrospective clinico-pathological analysis of 78 cases of fatal subarachnoid hemorrhage (SAH) was carried out: 71% had a pathological diagnosis of pulmonary edema (PE), and of these 31% had a clinical diagnosis of PE. Patients with pathological PE were younger and died sooner after their SAH than those without. The incidence of PE fell with the passage of time following SAH, while the occurrence of pneumonia and embolism increased. There were hypoxemia and hypocapnia in both groups, more severe in the group that had pathological PE. The pathophysiology of neurogenic PE is discussed and possible therapeutic approaches indicated.
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PMID:Pulmonary edema following fatal aneurysm rupture. 69 Jun 77

Transcranial Doppler sonography (TCD) flow velocities and cerebral blood flow (CBF) measurements were evaluated in 14 patients who had suffered a major aneurysmal subarachnoid hemorrhage (SAH). Cerebrovascular reactivity to hypocapnia was evaluated simultaneously by the two methods. The measurements were performed under general anaesthesia preoperatively, within 72 hours after the bleed, during normocapnia and hypocapnia. There was poor correlation between absolute values of hemispheric CBF and corresponding TCD mean flow velocity. Controlled hyperventilation was associated with a significant decrease in CBF as well as TCD flow velocity (p less than 0.001). In terms of reactivity indices the correlation between the two methods was poor and not significant (r = 0.33, p = 0.09). The principal differences between the methods are discussed as well as the application of TCD in the evaluation of cerebrovascular reactivity.
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PMID:Simultaneous transcranial Doppler sonography and cerebral blood flow measurements of cerebrovascular CO2-reactivity in patients with aneurysmal subarachnoid haemorrhage. 190 54

Cerebral vasospasm occurs, following subarachnoid haemorrhage, in the majority of patients and is accompanied by cerebral ischaemia in 30%. The objectives of this article are to review (1) the effects of subarachnoid haemorrhage and vasospasm on cerebral blood flow (CBF); (2) the effects of induced hypotension and hypocapnia on CBF in these patients; (3) current therapy for cerebral ischaemia from vasospasm. The medical literature was searched using Index Medicus; for the period 1983-90 this search was done on a computer with the CD-ROM version of Index Medicus, Silver Platter. Papers were selected on the basis of validity and applicability to clinical practice; animal studies are included when human data is lacking. Cerebral vasospasm may decrease cerebral blood flow, disturb autoregulation and place the patient at risk for delayed cerebral ischaemia. Intraoperative induced hypotension and hypocapnia can decrease CBF further, although effects of either on outcome have not been evaluated. Calcium antagonists are effective for both the prevention and the treatment of delayed cerebral ischaemia. Of the mechanical treatments, systemic-arterial hypertension has the firmest scientific foundation, although this is frequently combined with haemodilution and blood volume expansion. There is a need for randomized clinical trials to assess the efficacy of these latter treatments.
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PMID:Haemodynamic considerations in the management of patients with subarachnoid haemorrhage. 206 13

The authors describe a method for Doppler ultrasound recording of flow velocity in the basilar artery of normal rabbits and rabbits with experimental subarachnoid hemorrhage (SAH). With this transcranial Doppler (TCD) model, clinical assumptions regarding flow velocity/cerebral blood flow (CBF) relationships, autoregulatory responses, and Doppler spectral waveform analysis can be tested under controlled conditions and compared with established methods of CBF measurement (hydrogen clearance). The time course of changes in flow velocity following SAH (cerebral vasospasm) is successfully demonstrated using the experimental TCD method. There are significant differences in the flow velocity and CBF responses to hypercapnia, hypocapnia, and trimethaphan-induced hypotension which indicate that TCD cannot be considered a simple alternative to CBF measurement for the study of cerebrovascular reactivity and cerebral autoregulation.
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PMID:Transcranial Doppler ultrasound studies of cerebral autoregulation and subarachnoid hemorrhage in the rabbit. 211 49

Nicardipine, a calcium channel antagonist derivative of dihydropyridine, is a cerebral vasodilatator used in the treatment of cerebral vasospasms induced by subarachnoid hemorrhage after rupture of intracranial aneurysm. Hypocapnia is a powerful vasoconstrictor of cerebral arteries, and antagonizes in the baboon the cerebral vasodilative effect of nimodipine, another derivative of dihydropyridine. The action of nicardipine in presence of hypocapnia was not yet study in human. The study of the interaction of nicardipine and hypocapnia on the cerebral arteries show that hypocapnia antagonizes the cerebral vasodilatator properties of nicardipine.
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PMID:[Effect of nicardipine on cerebral vasomotor activity in hypocapnia]. 212 14

CO2 reactivity of the brain vessels was investigated in 33 patients (Grade I-III after Hunt and Hess) with cerebral vasospasm after an aneurysmal subarachnoid haemorrhage (SAH) and after early operation within 72 hours. In all cases, transcranial Doppler sonography was used to measure flow velocities in the middle cerebral artery (MCA) and internal carotid artery (ICA) and vasomotor reactivity to CO2 changes. Vasospastic conditions lead to higher flow velocities through the narrow segment, lower peripheral stream resistance due to the post-stenotic pressure drop and lower vasodilating capacities of arterioles under hypercapnia. In severe vasospastic conditions, the peripheral stream bed is already maximally dilated and the hypercapnic response is weak. On the other hand, the peripheral vascular bed reacts normally to hypocapnia in all vasospastic situations. Our results point out two dangerous conditions of vasospastic disease: 1) exhaustion of peripheral vasodilating capacities, and 2) hyperventilatory therapy. Both of these situations can result in a reduction of CBF to brain tissue, mainly for two reasons: 1) In the former, a further increase in vasospasm cannot be compensated for anymore when the peripheral arterioles are maximally dilated, and 2) in the latter, hypocapnia produces a strong peripheral vasoconstrictor response with further reduction of CBF.
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PMID:CO2 reactivity of cerebral vasospasm after aneurysmal subarachnoid haemorrhage. 250 Aug 37

The chemistry, pharmacology, pharmacokinetics, adverse effects, dosage, and availability of nimodipine are discussed, and the clinical use of nimodipine in preventing and treating cerebral arterial spasm in patients with subarachnoid hemorrhage is reviewed. Nimodipine is a highly lipid-soluble dihydropyridine derivative that readily crosses the blood-brain barrier. In animal studies, nimodipine has been shown to be effective in increasing cerebral blood flow; preventing vasoconstriction attributable to sympathetic stimulation, hypocapnia, and hypertension; and improving neurological outcome after cerebral ischemia. Nimodipine is reported to be 90% protein bound; its half-life is approximately 13 hours, with substantial interpatient variability. Nimodipine has been studied in the prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. In four open trials, in which nimodipine was administered orally, intravenously, topically during surgery, or by intracarotid injection, and in two double-blind, placebo-controlled trials, neurological outcomes were improved in patients receiving the drug. However, in both sets of trials nimodipine had limited effects on cerebral arterial spasm. Although nimodipine can cause hypotension, no serious adverse reactions to the drug were reported in clinical trials in patients with subarachnoid hemorrhage. Based on limited data currently available, nimodipine appears to improve neurological outcome in patients with subarachnoid hemorrhage. However, its efficacy in preventing or treating cerebral arterial spasm in these patients seems to be limited.
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PMID:Use of nimodipine for prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. 332 39

Ten patients with intracerebral tumours (TC) and 13 patients with subarachnoid haemorrhage (SAH) from a ruptured cerebral arterial aneurysm were studied before intracranial surgery, and during a 3-h postoperative period. Cerebrospinal fluid pressure (CSFP) determined by an intraventricular (TC group) or intraspinal (SAH group) catheter, and mean arterial blood pressure (MABP) were recorded under neurolept anaesthesia (control) followed by isoflurane inhalation. These two measurements were performed during normocapnia. A third measurement was made during hypocapnia, with unchanged isoflurane concentration. After the experimental period, isoflurane remained the main anaesthetic agent throughout the surgical procedure. After recovery from anaesthesia, the patients were monitored with CSFP and blood pressure during the first postoperative hours, and the quality of breathing was assessed by hourly blood-gas analyses. The results show that isoflurane causes a 10-14% reduction of MABP with no further changes during hyperventilation. Mean CSFP increased 27% in the TC group, and 12% in the SAH group after isoflurane induction and decreased from these levels by 29% during hyperventilation in both groups. Consequently, the impact on cerebral perfusion pressure (CPP) by isoflurane was a 19% and 21% mean decrease in the TC and SAH group, respectively. Controlled hyperventilation reduced this effect by partially restoring control CPP values, with 8% and 14% increase, respectively. In the postoperative follow-up, all patients had normal breathing and blood pressure with low values of CSFP. It is concluded that isoflurane can be used in intracranial surgery with adequate safety if combined with controlled hyperventilation.
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PMID:The effect of isoflurane on cerebrospinal fluid pressure in patients undergoing neurosurgery. 334 70

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

In this study we report our clinical experience with supplementary thiopental loading, based on 30 patients undergoing surgery for intracranial aneurysm after a recent episode of subarachnoid haemorrhage. As standard procedure we used pentobarbitone induction, pancuronium relaxation, endotracheal intubation, maintenance with halothane 0.5%, N2O 66% in oxygen, fentanyl, and moderate hypocapnia. A thiopental load of up to 20 mg X kg-1 was supplied while the aneurysm was approached. Satisfactory and well-controlled hypotension was obtained in five cases after thiopental alone, and after thiopental and sodium nitroprusside (SNP) (means +/- s.d.) 1.3 +/- 0.9 microgram X kg-1 X min-1 in the remaining 25 patients. No ECG sign of myocardial ischaemia was observed. One disadvantage was a prolonged recovery period, which in some cases necessitated controlled ventilation for some hours. We conclude that thiopental loading can be used safely as a supplement to neuroanaesthesia for aneurysm surgery.
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PMID:Thiopental loading during controlled hypotension for intracranial aneurysm surgery. 649 3


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