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

Two patients are described with hypercapnia of 10 and 13 years duration. Both patients had papilloedema at different stages of their illness and one patient developed optic atrophy. Whether such changes are due to local retinal vascular changes, general change in cerebral vasculature or the result of raised intracranial pressure is unknown. A combination of all seems likely. Computerized axial tomography brain scan on Case 2 was compatible with cerebral oedema and the development of optic atrophy (Case 1) suggests cerebral oedema and consequent raised intracranial pressure as the major factor in the development of papilloedema in hypercapnic patients. Skull radiographic changes have not previously been reported in hypercapnia. The duration of the papilloedema is critical in the development of atrophy.
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PMID:Papilloedema and optic atrophy in chronic hypercapnia. 55 69

A consecutive series of ten patients with chronic bronchitis and hypercapnia were studied. All seven patients with chronic hypercapnia and one patient with intermittent hypercapnia showed evidence on skull radiographs of raised intracranial pressure. In five male and three female chronic bronchitics matched for age and ventilatory impairment, but without hypercapnia, no such radiological abnormalities were shown. The clinical significance and pathophysiology of this hitherto unreported finding is discussed. It would appear that in some cases the chronicity of hypercapnia may be diagnosed from a radiograph of the pituitary fossa.
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PMID:Chronic hypercapnia and radiological changes in the pituitary fossa. 74 95

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Raised intracranial pressure due to cerebral oedema is a major cause of death in fulminant hepatic failure and in the present study we have carried out a controlled clinical trial of continuous hyperventilation in the prevention of this complication. Twenty patients were electively hyperventilated to maintain PaCO2 between 3.5 and 5 kPa. In the other 35 patients mechanical ventilation was instituted only if severe hypoxia or hypercapnia occurred. Cerebral oedema, diagnosed clinically or by a rise in intracranial pressure to greater than 30 mm Hg, occurred in 85% of hyperventilated patients and in 86% of those not so treated. Although there was no significant reduction in the number of episodes of cerebral oedema in the hyperventilated patients (4.8 episodes/24 h) as compared with the controls (5.3 episodes/24 h), hyperventilation did appear to delay the onset of coning but on the basis of these results could not be recommended to be used routinely as a prophylactic measure in the prevention of cerebral oedema in this condition.
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PMID:Controlled hyperventilation in the prevention of cerebral oedema in fulminant hepatic failure. 308 22

In 60%-90% of cases head injury is a part of multisystem trauma and of very decisive importance for the post-traumatic prognosis. Hypoxia, hypercarbia, and hypotension increase the primary lesion and cause secondary brain damage. Therefore, emergency measures must be directed to the essentials of sustaining vital functions, i.e. intubation/ventilation/oxygenation and stabilization of the circulatory system. All trauma-specific measures should avoid additional increases in intracranial pressure or should decrease it if already elevated. Moderate hyperventilation not only causes cerebral vasoconstriction with a concomitant decrease in intracranial blood volume and intracranial pressure, but also partly restores the disturbed cerebral autoregulation, and is therefore an important part of the emergency care and anesthetic procedure in patients with severe head injuries. It is supplemented by analgesia and sedation to prevent intracranial pressure increases due to painful external stimuli. Elevation of the head and upper part of the body by 30 degrees causes a decrease in intracranial pressure by decreasing intracranial blood volume due to improved venous return from the brain; however, this measure is to be applied only in stable circulatory conditions. The head should be put in mid-position avoiding sideways rotation, flexion, and hyperextension. Osmotically active agents are only indicated in emergency situations when there are signs of clinical deterioration. High-dose barbiturate therapy is reserved as a "last resort", under intensive care conditions, for controlling an otherwise intractable intracranial pressure rise. Calcium antagonists have no indication in this context. Anesthesia in patients with severe head injury must involve only those techniques that do not further increase an already elevated intracranial pressure. As inhalational anesthetics, including nitrous oxide, elevate the intracranial pressure to varying extents due to cerebral vasodilation with a concomitant rise in intracranial blood volume, these substances have to be avoided whenever raised intracranial pressure cannot be excluded. Narcotics, benzodiazepines, small dosages of barbiturates, and long-lasting muscle relaxants can be regarded as useful.
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PMID:[Pathophysiologic principles, emergency medical aspects and anesthesiologic measures in severe brain trauma]. 331 Jul 24

Fourteen male patients with chronic bronchitis and hypoxia had a lateral radiograph of the pituitary fossa. Nine of the 14 had definite or probable abnormalities, a significantly higher frequency (p less than or equal to 0.01) than is represented by the two out of 14 age-matched men from a control group with head injuries. The most common change was thinning or erosion of the lamina dura. Patients with hypercapnia were no more prone to such abnormalities than were those with normocapnia, a finding that conflicts with a previous paper. We confirm that radiological pituitary fossa changes do occur in chronic bronchitis, that they are unrelated to steroid treatment, and that they are probably not solely due to the chronically raised intracranial pressure associated with hypercapnia. Other possible mechanisms are discussed--in particular hypoxia, which might produce changes on account of the increased cerebral blood flow and engorged intracranial blood vessels.
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PMID:Radiological pituitary fossa changes in chronic bronchitis. 713 92

To successfully match the treatment to the cause for raised intracranial pressure (ICP) after a severe head injury, it is important to know the underlying mechanism at a given moment for the raised pressure. In particular, it is important to distinguish between active cerebral vasodilation, indicating functional autoregulation, and a passive vascular dilation as the cause for raised ICP. An experimental study was performed in feline models of diffusely raised ICP (n = 6), of active arterial vasodilation caused by arterial hypercarbia (n = 6), and of passive arterial dilation caused by pharmacologically induced arterial hypertension (n = 6) to determine if wave form analysis of ICP can distinguish active from passive arteriolar vasodilation. Pulsatile pressure transmission from the blood pressure pulse to the ICP pulse (cerebrovascular pressure transmission [CVPT]), cerebrovascular resistance, and craniospinal compliance were measured simultaneously at each level of raised ICP, arterial hypercarbia, and arterial hypertension. Arterial hypercarbia, caused by both 5 and 10% inspired CO2 increased low-frequency CVPT, which was followed by an increasingly negative phase shift between the blood pressure and ICP wave form (P < 0.05). Diffusely raised ICP caused by intraventricular infusion of mock cerebrospinal fluid caused increased low-frequency CVPT (P < 0.01) but resulted in no overall change in phase shift, although the sign of the phase shift remained negative. After arterial hypertension, caused by the infusion of angiotensin II, where there was loss of myogenic tone, an increased low-frequency CVPT was accompanied by a positive phase shift (P < 0.01). These data demonstrate it may be possible to distinguish active arteriolar vasodilation from a passive loss of autoregulatory vascular tone through simultaneous measurement of the low-frequency CVPT and phase shift. Analysis of the ICP wave form provides information relevant to the management of raised ICP.
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PMID:An experimental study of cerebrovascular resistance, pressure transmission, and craniospinal compliance. 812 65

Clinical studies with transcranial Doppler suggest that the pulsatility of the flow velocity (FV) waveform increases when the distal cerebrovascular resistance (CVR) increases. To clarify this relationship, the authors studied animal models in which the resistance may be decreased in a controlled manner by an increase in arterial CO2 tension, or by a decrease in cerebral perfusion pressure (CPP) in autoregulating animals. Twelve New Zealand white rabbits were anesthetized, paralyzed, and ventilated. Transcranial Doppler basilar artery FV, laser Doppler cortical blood flow, arterial pressure, intracranial pressure, and end-tidal CO2 concentration were measured continuously. Cerebrovascular resistance (CPP divided by laser Doppler cortical flux) and Gosling Pulsatility Index (PI, defined as an FV pulse amplitude divided by a timed average FV) were calculated as time-dependent variables for each animal. Four groups of animals undergoing controlled manipulations of CVR were analyzed. In Group I, arterial CO2 concentration was changed gradually from hypocapnia to hypercapnia. In Group II, gradual hemorrhagic hypotension was used to reduce CPP. In Group III, the short-acting ganglion blocking drug trimetaphan was injected intravenously to induce transient hypotension. Intracranial hypertension was produced by subarachnoid saline infusion in Group IV. During the hypercapnic challenge the correlation between the cortical resistance and Doppler flow pulsatility was positive (r = 0.77, p<0.001). In all three groups in which cerebral perfusion pressure was reduced a negative correlation between pulsatility index and cerebrovascular resistance was found (r = -0.84, p<0.001). The authors conclude that PI cannot be interpreted simply as an index of CVR in all circumstances.
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PMID:Relationship between transcranial Doppler-determined pulsatility index and cerebrovascular resistance: an experimental study. 861 40

Increased intracranial pressure can be a catastrophic event that may lead to death or permanent disability. Without prompt recognition and reversal of hypoxia, hypotension, hypercarbia, acidosis and increased intracranial pressure, the cerebral blood flow and resultant cerebral perfusion can be inadequate, leading to an exacerbation of secondary brain injury.
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PMID:Beyond the basics: brain injuries. 1767 75

A young man sustained traumatic lung, head and abdominal injuries. Despite mechanical ventilation, deteriorating respiratory function resulted in severe hypoxia and hypercapnia, with high P(a)co(2) compounding an already raised intracranial pressure (ICP). The Novalung was pre-emptively used without anticoagulation, prior to laparotomy, to remove carbon dioxide and to allow for cerebral and lung protective strategies. This facilitated control of ICP thereby limited possible secondary brain injury.
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PMID:Pre-emptive Novalung-assisted carbon dioxide removal in a patient with chest, head and abdominal injury. 1858 63


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