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

The impedance of a hemodynamic system is defined as the ratio of each harmonic component of blood pressure to that of flow. Calculation of impedance cures has been extensively performed in the systemic circulation, leading to the recognition of reflected pressure and flow waves and clarifying the shape of ultrasound waveforms. Impedance in the human cerebral circulation has not been measured primarily because of the relative inaccessibility of simultaneous flow and pressure data in the human cerebral circulation. We defined an impedance index using the transcranial Doppler waveform for that of flow and a noninvasive applanation measure of the carotid artery pressure waveform. Middle cerebral artery velocities and carotid artery pressure waveforms were simultaneously recorded in 16 vessels from 10 normal volunteers, 42 vessels in 14 patients with aneurysmal subarachnoid hemorrhage, and 14 vessels in 7 subjects during conditions of hypocapnia, normocapnia and hypercapnia. Impedance was calculated by dividing the harmonic associated with pressure divided by that of flow, and averaging 10 to 20 such calculations. Relative impedance curves were calculated by dividing by the impedance at the first harmonic. Impedance was also studied in an electrical model consisting of a Windkessel element containing inductance in series with a second Windkessel to model the large vessel and vascular bed, respectively. Model parameters were taken from the literature for these calculations. For the normal subjects, the shape of the impedance index curve was similar to those found in the systemic circulation. The impedance index curves for patients in vasospasm (middle cerebral velocity was greater than 180) showed a peak at the second or third harmonic, which appeared more frequently than the nonspasm group (p < 0.01). Furthermore, the ratio of the second harmonic to the first harmonic was significantly > 1.0 in the spasm group but significantly < 1.0 in the normal group (p < 0.05). Calculations from the electrical model replicated the appearance of these peaks at the second or third harmonic for vasospasm parameters. A statistically significant peak appeared at the second or third harmonic in the impedance index curves for patients in vasospasm, which was replicated quantitatively by our electrical model. Although such peaks can be explained in the systemic circulation by the presence of reflected waves, the distance to the reflection site is larger than expected for the cerebral circulation. This suggests the importance of the inertia of blood as a stenosis worsens and as the origin for the observed changes in the impedance index curves.
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PMID:An impedance index in normal subjects and in subarachnoid hemorrhage. 1105 55

1. Mechanisms that regulate the cerebral circulation have been intensively investigated in recent years. The role of several vasodilator mechanisms has been examined in the cerebral circulation, including nitric oxide (NO), trigeminal peptides and potassium channels, as well as the potent vasoconstrictor endothelin. These mediators appear to play a role in physiological and pathophysiological responses of the cerebral circulation. In the present review, we will focus on some recent developments in each of these areas. 2. Nitric oxide is an important regulator of cerebral vascular tone. Tonic production of NO maintains the cerebral vasculature in a dilated state. NO appears to be an important vasodilator during activation of neurons by excitatory amino acids, somatosensory stimulation and cortical spreading depression. Tonic production of NO appears to be critical in vasodilatation during hypercapnia, although NO may not directly mediate vasodilatation. NO produced by immunological NO-synthase appears to be important in dilatation following exposure to bacterial endotoxin. 3. Calcitonin gene-related peptide (CGRP), released from trigeminal perivascular sensory nerves in the brain, is an extremely potent dilator of brain vessels. CGRP may limit noradrenaline-induced constriction of cerebral vessels and contribute to dilatation during hypotension (autoregulation), reactive hyperaemia, seizures and cortical spreading depression. 4. Activation of potassium channels leads to hyperpolarization of cerebral vascular smooth muscle and appears to be a major mechanism for dilatation of cerebral arteries. Agents that increase the intracellular concentration of cyclic 3' 5'-adenosine monophosphate (cAMP) produce vasodilatation in part by activation of large conductance calcium-activated potassium channels (BKCa) and ATP-sensitive potassium channels (KATP). Activation of both KATP and BKCa channels also appears to contribute to vasodilatation during hypoxia. In contrast to KATP channels, BKCa channels appears to be active under basal conditions, contributing to tonic dilatation of cerebral blood vessels. 5. Endothelin is produced in the brain, but its role in the physiological regulation of cerebral blood flow is not known. Endothelin may contribute to the spasm of cerebral arteries following subarachnoid haemorrhage.
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PMID:Recent insights into the regulation of cerebral circulation. 880 May 65

Seizures and convulsive status in patients with subarachnoid haemorrhage are an emergency. They are not only known to increase cerebral metabolic rate but also cerebral blood flow and intracranial pressure and rebleeding can occur in patients with an unclipped aneurysm. The goal of therapy is to stop the seizures minimizing the risk of secondary brain damage (hypoxia, hypotension, hypercarbia, hyperthermia). Several active drugs are available for treating seizures, it is important to identify the cause, prompt administration, monitoring the patients and choosing the one with less side effects.
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PMID:[Seizures associated with acute subarachnoid hemorrhage. Emergency diagnosis and treatment]. 977 39

In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an Intensive Care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.
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PMID:Subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma. 1059 94

There is no question that substantial progress has been made over the last 30 years, since the pioneering multinational studies of Jennett and colleagues, in our understanding of the mechanisms involved in the production, progression, and amelioration of brain damage. The introduction of computed tomography and simple but elegant classifications of the severity of injury (e.g., the Glasgow Coma Scale and the Glasgow Outcome Scale) were seminal milestones in neurotraumatology. When neurosurgeons such as Langfitt, Becker, and Miller took advantage of the pioneering investigations of intracranial hypertension by Janny and Lundberg and combined them with imaging, classification of brain damage, and improvements in emergency medical services, substantial gains were soon made. However, given the perspective of the beginning of the 21 st century, one can see those gains as relatively straightforward, as they have required the consolidation of concepts and ideas that fit together relatively easily. Better attention to easily delineated abnormalities, such as shock, hypoxia, and hypercarbia, and the early evacuation of mass lesions coupled with the concurrent development of modern principles of critical care account for substantial reductions in mortality and a reduction in the number of vegetative, contracted, spastic survivors. Future improvement in the care of patients with head injuries will increasingly be dependent on advances in molecular neurobiology and psychology, our ability to successfully modulate genetic expression, and progress in the treatment of related illnesses, such as stroke, subarachnoid hemorrhage, depression, and Alzheimer's disease.
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PMID:Head injury: recent past, present, and future. 1098 41

A 45-year-old woman underwent radical neck clipping for cerebral aneurysm under isoflurane anesthesia. Her preoperative examination revealed elevated body temperature which had been normal on admission. Her body temperature increased up to 40.3 degrees C during anesthesia and surgery, and it showed a downward trend at the end of surgery. Malignant hyperthermia was excluded because the patient did not have metabolic acidosis, hypercarbia, hyperpotassemia or abnormal sweating anesthesia. The patient received intravenous dantrolene postoperatively since there was a suspicion of malignant hyperthermia on the basis of hyperthermia and increases in serum creatine kinase (CK) and myoglobin (Mb) levels. Her body temperature and serum CK and Mb levels decreased for a while after administration of dantrolene, but they increased again thereafter. The patient was aggressively cooled with a cooling blanket and hyperthermia and increases in serum CK and Mb levels disappeared in postoperative two weeks. She was discharged on foot without any neurological deficit on the forty-third hospital day. According to the diagnostic criteria for malignant hyperthermia by Larach and his colleague, malignant hyperthermia was somewhat less than likely in our case. The clinical course of the patient also suggested that a possibility of malignant hyperthermia was considerably low. The authors conclude that perioperative hyperthermia in our case must have derived from central hyperthermia following subarachnoid hemorrhage, and that postoperative increases in serum CK and Mb levels might have resulted from acceleration of sympathetic nervous system by subarachnoid hemorrhage.
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PMID:[Central hyperthermia suspected of malignant hyperthermia in a patient undergoing radical neck clipping for cerebral aneurysm]. 1571 69

We developed a rat cerebral angiography system using monochromatic synchrotron radiation X-rays at SPring-8, a third generation synchrotron radiation facility. Using new technique, we assessed the distensibility of major trunk arteries after subarachnoid hemorrhage (SAH) in normotensive and hypertensive rats. Twenty-five adult Wistar Kyoto rats (WKY) and fourteen stroke-prone spontaneously hypertensive rats (SHR) were prepared SAH by double hemorrhage injection method into cisterna magna. Angiography was performed on day 7 and was repeated three times in each rat before and after loading of hypercapnia at 100-120 mmHg of PaCO2. The diameters of major trunk vessels were assessed. Light microscopic observation of artery lumen and wall were also performed. Angiographical vasospasm was demonstrated in basilar artery in WKY with 66 % reduction in diameter of control. In ICA and other major trunk in WKY and all the arteries in SHR did not demonstrate vasospasm. SHA resulted in loss of hypercapnia-induced distention in BA of WKY. In SHR, the distensibility was impaired regardless of hemorrhage. Histological study demonstrated basilar artery in WKY thickened at 184 % after SAH and became similar to non-hemorrhagic SHR. ICA in WKY and both BA and ICA in SHR were unchanged in wall thickness before and after SAH. High quality angiography demonstrated deteriorated distensibility in chronic hypertension or SAH-induced spastic vessels.
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PMID:Loss of CO2-induced distensibility in cerebral arteries with chronic hypertension or vasospasm after subarachnoid hemorrhage. 1876 26

Cerebral blood flow (CBF) is regulated by vasomotor, chemical, metabolic, and neurogenic mechanisms. Even though the innervation of cerebral arteries is quite extensively described and reviewed in the literature, its role in regulation of CBF in humans remains controversial. We believe that insufficient attention has so far been focused on the potential role of the innervation of the cerebral vasculature in cerebral autoregulation in humans. We have performed an extensive search and selection of available literature on electrical, chemical, and surgical manipulations of the sympathetic innervation of cerebral arteries, and the effects of circulation sympathetically active agents on CBF. Studies on (surgical) ganglion block show a role of sympathetic tone in preventing increases in CBF in humans, which are consistent with the view based on animal studies. Both direct innervation of the cerebral arteries from cervical ganglia and stimulation of adrenergic receptors by circulating sympathomimetics prevent sudden increases of CBF associated with hypertension and hypercapnia. We postulate that under normal physiological conditions neurogenic control has little influence on cerebral autoregulation as other methods of control (vasomotor, chemical, and metabolic) are dominant. In severely challenging circumstances, such as delayed cerebral ischaemia after subarachnoid haemorrhage, these methods might be overwhelmed, increasing the relative importance of neurogenic, sympathetic control of CBF. This insight might lead to future therapeutic possibilities.
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PMID:Sympathetic regulation of cerebral blood flow in humans: a review. 2361 89

A 46-year-old man developed central respiratory failure in the subacute phase of unilateral lateral medullary infarction. He complained of sudden headache and nausea at first. Neurological examination revealed Wallenberg's syndrome. Acute right lateral medullary infarction caused by the dissecting right vertebral artery was identified by magnetic resonance images. He was transferred to our hospital on the 3rd day after the onset. He was alert and conscious on admission, and became restless gradually later. He was intubated for sudden respiratory failure on the 9th day. Blood gas analysis showed hypercapnia and hypoxia. Central respiratory failure was indicated by the fact that various examinations showed no change of his infarction, no subarachnoid hemorrhage, or no worsening of pneumonia. Ventilatory support was required for a month because of repetitive CO2 narcosis. He was weaned from the ventilator on the 39th day. Only a few reports are available on central respiratory failure associated with the subacute phase of unilateral medullary infarction. Delayed central respiratory failure may be lethal. Careful observation is required on the subacute phase of Wallenberg's syndrome.
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PMID:[Central respiratory failure occurred in the subacute phase of unilateral Wallenberg's syndrome: a case report]. 2480 72

Increasing evidence indicates that poor outcomes after brain hemorrhage, especially after subarachnoid hemorrhage (SAH), can be attributed largely to dysfunction of the cerebral microcirculation. However, the cause of this dysfunction remains unclear. Here, we investigated changes in the cerebral microcirculation after regional hemorrhage in the subarachnoid space using the closed cranial window technique in mice. A single pial arteriole on the surface of the brain was punctured to induce a regional hemorrhage in the subarachnoid space. Physiological parameters were monitored during the procedure, and microvessel diameter was measured after hemorrhage. The vasoreactivity of the arterioles in response to hypercapnia as well as to topical application of the vasodilator acetylcholine (ACh) and S-nitroso-N-acetyl-penicillamine (SNAP) were assessed. The constriction of pial arterioles was detected without changes in other physiological parameters. Decreased reactivity of pial arterioles to all of the applied vasodilatory stimuli was observed after hemorrhage. Our results indicate that regional hemorrhage in the subarachnoid space can induce the vasospasm of microvessels and also reduce the vasoreactivity of pial arterioles.
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PMID:Constriction and dysfunction of pial arterioles after regional hemorrhage in the subarachnoid space. 2559 4


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