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

Monitoring of brain tissue partial pressure of O2 (ti-pO2) is a promising new technique that allows early detection of impending cerebral ischemia in brain-injured patients. The purpose of this study was to investigate the effects of standard therapeutic interventions used in the treatment of intracranial hypertension in comatose patients on cerebral oxygenation. In the neurosurgical intensive care unit ti-pO2, arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO2) were prospectively studied (0.1 Hz acquisition rate) in 23 comatose patients (21 with severe traumatic brain injury, 2 with intracerebral hematoma) during various treatment modalities: elevation of CPP with dopamine (n = 35), lowering of the head (n = 22), induced arterial hypocapnia (n = 13), mannitol infusion (n = 16), and decompressive craniotomy (n = 1). Ischemic episodes ('IE' = ti-pO2 < 10 mmHg for > 15 min) within the first week after the insult were always associated with unfavorable neurological outcome. Elevation of CPP from 32 +/- 2 to 67 +/- 4 mmHg significantly improved ti-pO2 by 62% (13 +/- 2 to 21 +/- 1 mmHg) and reduced ICP indicating intact cerebral autoregulation. Further raising CPP from 68 +/- 2 to 84 +/- 2 mmHg did not alter ti-pO2. Mannitol-induced ICP reduction from 23 +/- 1 to 16 +/- 2 mmHg did not affect ti-pO2, nor did lowering of the head from 30 degrees to 0 degree. Hyperventilation from an endtidal pCO2 of 29 +/- 3 to 21 +/- 3 mmHg normalized ICP and CPP, but significantly reduced ti-pO2 from 31 +/- 2 to 14 +/- 3 mmHg. Decompressive craniotomy in a 15-year old patient with refractory intracranial hypertension instantly restored ti-pO2. Based on the present data, our understanding of many interventions previously believed to improve brain oxygenation might have to be re-evaluated. A CPP > 60 mmHg emerges as the most important factor determining sufficient brain tissue pO2. Any intervention used to further elevate CPP does not improve ti-pO2, to the contrary, hyperventilation even bears the risk of inducing brain ischemia.
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PMID:Brain tissue pO2-monitoring in comatose patients: implications for therapy. 919 72

We previously have demonstrated that hypocapnia aggravates and hypercapnia protects the immature rat from hypoxic-ischemic brain damage. To ascertain cerebral blood flow (CBF) and metabolic correlates, 7-d postnatal rats were subjected to hypoxia-ischemia during which they were rendered either hypo-(3.5 kPa), normo- (5.1 kPa), or hypercapnic (7.3 kPa) by the inhalation of either 0, 3, or 6% CO2, 8% O2, balance N2. CBF during hypoxia-ischemia was better preserved in the normo- and hypercapnic rat pups; these animals also exhibited a stimulation of cerebral glucose utilization. Brain glucose concentrations were higher and lactate lower in the normo- and hypercapnic animals, indicating that glucose was consumed oxidatively in these groups rather than by anaerobic glycolysis, as apparently occurred in the hypocapnic animals. ATP and phosphocreatine were better preserved in the normo- and hypercapnic rats compared with the hypocapnic animals. Cerebrospinal fluid glutamate, as a reflection of the brain extracellular fluid concentration, was lowest in the hypercapnic rats at 2 h of hypoxia-ischemia. The data indicate that during hypoxia-ischemia in the immature rat, CBF is better preserved during normo- and hypercapnia; the greater oxygen delivery promotes cerebral glucose utilization and oxidative metabolism for optimal maintenance of tissue high energy phosphate reserves. An inhibition of glutamate secretion into the synaptic cleft and its attenuation of N-methyl-D-aspartate receptor activation would further protect the hypercapnic animal from hypoxic-ischemic brain damage.
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PMID:Effect of carbon dioxide on cerebral metabolism during hypoxia-ischemia in the immature rat. 921 33

Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). CO2-reactivity and CBF was estimated using AVDO2 (arteriojugular differences of oxygen content). Global cerebral ischemia and increased anaerobic metabolism were considered according to AVDO2 and AVDL respectively. Thirty-three patients with severe and moderate head injury and increased ICP were included. Within 72 hours after accident, patients were hyperventilated for a period of 4 hours. During this time jugular oxygen saturation (SjO2), arterial oxygen saturation (SaO2), ICP, mean arterial blood pressure (MABP), AVDO2 and AVDL were recorded. In our study, most patients preserved CO2-reactivity (88.2%). In these cases HV was very effective in lowering ICP. Our findings showed that this reduction was due to a CBF decrease. According to basal AVDO2 twenty-five patients (75.7%) were considered as hyperemic and eight (24.2%) as not hyperemic. Global ischemia and increased anaerobic metabolism were detected in one case in the non-hyperemic group. According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.
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PMID:Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia? 977 27

A unique method for simultaneously measuring interstitial (pHe) as well as intracellular (pHi) pH in the brains of lightly anesthetized rats is described. A 4-mm microdialysis probe was inserted acutely into the right frontal lobe in the center of the area sampled by a surface coil tuned for the collection of 31P-NMR spectra. 2-Deoxyglucose 6-phosphate (2-DG-6-P) was microdialyzed into the rat until a single NMR peak was detected in the phosphomonoester region of the 31P spectrum. pHe and pHi values were calculated from the chemical shift of 2-DG-6-P and inorganic phosphate, respectively, relative to the phosphocreatine peak. The average in vivo pHe was 7.24+/-0.01, whereas the average pHi was 7.05+/-0.01 (n = 7). The average pHe value and the average CSF bicarbonate value (23.5+/-0.1 mEq/L) were used to calculate an interstitial Pco2 of 55 mm Hg. Rats were then subjected to a 15-min period of either hypercapnia, by addition of CO2 (2.5, 5, or 10%) to the ventilator gases, or hypocapnia (PCO2 < 30 mm Hg), by increasing the ventilation rate and volume. pHe responded inversely to arterial Pco2 and was well described (r2 = 0.91) by the Henderson-Hasselbalch equation, assuming a pKa for the bicarbonate buffer system of 6.1 and a solubility coefficient for CO2 of 0.031. This confirms the view that the bicarbonate buffer system is dominant in the interstitial space. pHi responded inversely and linearly to arterial PCO2. The intracellular effect was muted as compared with pHe (slope = -0.0025, r2 = 0.60). pHe and pHi values were also monitored during the first 12 min of ischemia produced by cardiac arrest. pHe decreases more rapidly than pHi during the first 5 min of ischemia. After 12 min of ischemia, pHe and pHi values were not significantly different (6.44+/-0.02 and 6.44+/-0.03, respectively). The limitations, advantages, and future uses of the combined microdialysis/31P-NMR method for measurement of pHe and pHi are discussed.
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PMID:In vivo microdialysis of 2-deoxyglucose 6-phosphate into brain: a novel method for the measurement of interstitial pH using 31P-NMR. 988 94

We investigated the adverse effect of hypocapnia on the neonatal rabbit brain. Two-week-old Japanese white rabbits were assigned to three groups, hyperventilation (H group), ischemia (I group), or hypocapnia with ischemia (HI group) and then subjected for 1.5 h with simultaneous measurement of the mean arterial blood pressure (MABP) and intracranial Hb concentration changes. Marked reductions of PaCO2 and MABP were induced in the hyperventilation-loaded groups and the ischemia-loaded groups, respectively. The intracranial oxyhemoglobin and total Hb concentrations decreased slightly in the H group and markedly in the I and HI groups after the start of experimental protocols, although there were no statistical differences between the I and HI groups. Animals were killed at 24 h after experiments and then subjected to pathologic examination. Damaged neurons with shrunken cell bodies and nuclear changes were found on light microscopic examination, mainly in the pyramidal cell layer of the subiculum and cornu ammonis 1. The numerical density of damaged neurons was significantly higher in the HI group than those in the H or I groups (p < 0.05). These damaged neurons were positive on DNA nick end labeling. A DNA ladder was detected on electrophoresis with a DNA sample extracted from hippocampal tissue in the HI group, but not in the other two groups. On electron microscopic examination, not only condensation of the nucleus but also disruption of mitochondria and the cell membrane were detected. These results suggested that hypocapnia under hypotension might cause neuronal cell death in the hippocampus of neonatal rabbit. Not only ischemia but also a metabolic change induced by hypocapnia might contribute to this apoptotic neuronal cell damage.
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PMID:Hypocapnia under hypotension induces apoptotic neuronal cell death in the hippocampus of newborn rabbits. 1087 96

Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia-reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (FI(CO(2)) = 0.06) or groups with hypocapnia (FI(CO(2)) = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchanged in the control group but were elevated in the group with hypocapnia; elevation in microvascular permeability was greater in the hypocapnia versus control groups. Injury following ischemia-reperfusion was significantly worse in the hypocapnia versus control groups. In a preliminary series, degree of lung injury was proportional to the degree of hypocapnic alkalosis. We conclude that in the current model (1) hypocapnic alkalosis is directly injurious to the lung and (2) hypocapnic alkalosis potentiates ischemia-reperfusion-induced acute lung injury.
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PMID:Injurious effects of hypocapnic alkalosis in the isolated lung. 1093 60

Chronic prophylactic hyperventilation therapy should be avoided during the first 5 days after severe TBI and particularly during the first 24 h. CBF measurements in patients with severe TBI demonstrate that blood flow early after injury is low and strongly suggest that in the first few hours after injury the absolute values approach those consistent with ischemia. These findings are corroborated by AVdO2 and SjO2 and brain tissue O2 measurements. Hyperventilation will reduce CBF values even further, but will not consistently cause a reduction of ICP and may cause loss of autoregulation. The cerebral vascular response to hypocapnia is reduced in those with the most severe injuries (subdural hematomas and diffuse contusions), and there is substantial local variability in perfusion. While the CBF level at which irreversible ischemia occurs has not been clearly established, ischemic cell change has been demonstrated in 90% of those who die following TBI, and there is PET evidence that such damage is likely to occur when CBF drops below 15-20 cc/100 g/min. A prospective randomized clinical trial has determined that outcomes are worse when TBI patients are treated with chronic prophylactic hyperventilation therapy. Within the standard, guideline, and options, specific paCO2 thresholds have been described that are different for each of the three parameters. These individual thresholds were selected based on the preponderance of literature supporting those thresholds in the contexts of the statements which included them. With the exception of the threshold included for the standard in this guideline, it is emphasized that the paCO2 threshold is not as important as the general concept of hyperventilation. The preponderance of the physiologic literature concludes that hyperventilation during the first few days following severe traumatic brain injury, whatever the threshold, is potentially deleterious in that it can promote cerebral ischemia.
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PMID:The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Hyperventilation. 1093 94

In vivo mammalian preparations can exhibit eupnea, apneusis and gasping. In vitro mammalian preparations exhibit only a single invariant pattern, which appears identical to gasping. We characterized the patterns of ventilatory activity of a perfused heart-brainstem preparation of the juvenile rat. In this preparation, phrenic activity has a 'ramp-like' rise similar to eupnea in vivo. Peak phrenic activity declines and ultimately disappears in hypocapnia. In hypercapnia, both frequency and peak of phrenic bursts increase. In hypoxia, such increases are transient. The phrenic burst is terminated by electrical stimulation of the pontile 'pneumotaxic center' and, as in apneusis, is prolonged by lesions in this region. With severe hypoxia or ischemia, the 'ramp-like' phrenic activity is replaced by the 'decrementing' pattern of gasping. Variables of phrenic activity in gasping produced in hypoxia and ischemia are identical. We conclude that the perfused juvenile rat preparation exhibits patterns of eupnea, apneusis and gasping which are similar to in vivo mammalian preparations.
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PMID:Characterizations of eupnea, apneusis and gasping in a perfused rat preparation. 1100 87

Anesthesia may be an important factor in maximizing the success of microsurgery by controlling the hemodynamics and the regional blood flow. The intraanesthetic basic goal is to maintain an optimal blood flow for the vascularized free flap by: increasing the circulatory blood flow, maintaining a normal body temperature to avoid peripheral vasoconstriction, reducing vasoconstriction resulted from pain, anxiety, hyperventilation, or some drugs, treating hypotension caused by extensive sympathetic block and low cardiac output. A hyperdynamic circulation can be obtained by hypervolemic or normovolemic hemodilution and by decrease of systemic vascular resistance. The importance of proper volume replacement has been widely accepted, but the optimal strategy is still open to debate. General anesthesia combined with various types of regional anesthesia is largely preferred for microvascular surgery. Maintenance of homeostasis through avoidance of hyperoxia, hypocapnia, and hypovolemia (all factors that can decrease cardiac output and induce local vasoconstriction) is a well-established perioperative goal. As the ischemia-reperfusion injury could occur, inhalatory anesthetics as sevoflurane (that attenuate the consequences of this process) seem to be the anesthetics of choice.
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PMID:Anesthesia for free vascularized tissue transfer. 1894 83

The main purpose of neurointensive care is to fight against cerebral ischaemia. Ischaemia is the cell energy failure following inadequacy between supply of glucose and oxygen and demand. Ischemia monitoring starts with a global approach, especially with cerebral perfusion pressure (CPP) determined by mean arterial pressure and intracranial pressure (ICP). However, global monitoring is insufficient to detect "regional" ischaemia, leading to development of local monitoring such as brain oxygen partial pressure (PtiO(2)). PtiO(2) is measured on a volume of a few mm(3) from a probe implanted in the cerebral tissue. The normal value is classically included between 25 and 35 mmHg and critical ischemic threshold is 10 mmHg. Understanding what exactly is PtiO(2) is still a matter of debate. PtiO(2) is more an indicator of oxygen diffusion depending of oxygen arterial pressure (PaO(2)) and local cerebral blood flow (CBF). Increase PaO(2) to treat PtiO(2) would hide information about local CBF. PtiO(2) is useful for the detection of low local CBF even when ICP is low as in hypocapnia-induced vasoconstriction. PtiO(2)-guided management could lead to a continuous optimization of arterial oxygen transport for an optimal cerebral tissue oxygenation. Finally, PtiO(2) has probably a global prognostic value because studies showed that hypoxic values for a long period of time lead to an unfavourable neurologic outcome. In conclusion, PtiO(2) provides additional information for regional monitoring of cerebral ischaemia and deserves more intensive use to better understand it and probably improve neurointensive care management.
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PMID:[Brain tissue oxygen pressure, for what, for whom?]. 2269 87


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