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Query: HUMANGGP:003739 (CO2)
 48,959 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In industrial countries the symptoms "headache" has an incidence of about 10%, and hypertension between 20 and 25%. Both terms are summary and may be pointers to and warning signals of the most varied disease processes. While, in malignant hypertensions, and pheochromocytoma, headache is a cardinal symptom, its causal connection with permanently raised blood pressure in the "benign" forms is viewed with scepticism. The observation that hypertensives frequently complain of headaches with a maximum intensity in the early hours of the morning is connected with the fall in blood pressure with accumulation of CO2 in shallow breathing. Headache as a symptom characteristic of hypertension is frequently only facultative in nature and must be classified among the series of symptoms of sequelae. But it offers a sufficient reason to institute a selective examination programme, especially as hypertension is still the most common cause of death even today.
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PMID:[Headache associated with hypertension from the internist's and neurologist's point of view (author's transl)]. 81 25

A case of primary Intracranial Hypotension (PIH) is described. This syndrome consists of spontaneous lowering of CSF pressure with traction headache. It is a benign disorder and is self-limited. The cause is unknown, but local choroid plexus vasospasm, possibly due to a hypothalamic disturbance, has been suggested, as has leakage of CSF through spontaneous arachnoid tears. Transient symptomatic relief was achieved with 5% CO2 inhalation, apparently due to increase in cerebral blood flow.
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PMID:Primary intracranial hypotension: the syndrome of spontaneous low cerebospinal fluid pressure with traction headache. 83 25

A syndrome of alveolar hypoventilation has been identified in a group of patients with bilateral diaphragm paralysis. Eight patients were studied in whom diaphragm weakness had been suggested by paradoxical (inward) movement of the abdominal wall on inspiration, of whom seven had evidence of a generalized neuromuscular disorder. Diaphragm function was assessed quantitatively by measurement of the change in transdiaphragmatic pressure during a maximum inspiration (deltaPDi). In five patients, deltaPDi was zero and in the others ranged from 2-6 cm H2O (normal greater than 25 cm H2O) indicating paralysis and severe weakness in the respective groups. Fluoroscopy of the diaphragm was found to give misleading results, and the resons for this are considered. Vital capacity ranged from 65-30 per cent of the predicted normal in the upright posture, typically falling by about a half in the supine posture. Alveolar hypoventilation was present in five patients when supine and in six when asleep, the deterioration in blood gases associated with sleep generally being much greater in these patients than in normal subjects. Respiratory rate was significantly greater than age-matched controls. The ventilatory response to CO2 was impaired. The PCO2 could be brought to normal levels by voluntary hyperventilation, and the unreliability of voluntary respiratory manoeuvres of this kind as indices of ventilatory reserve is emphasized. Alveolar hypoventilation was associated with disturbed sleep, morning headache and day-time fatigue. Symptomatic benefit was achieved by the use of a cuirass respirator at night.
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PMID:Diaphragm function and alveolar hypoventilation. 106 15

In this study, blood flow velocity in the basilar artery and both vertebral and middle cerebral arteries was measured with a transcranial Doppler device in 23 migraineurs during and outside a migraine attack. The aim of the study was to compare blood flow velocities during and outside an attack and to examine vascular reactivity to voluntary hyperventilation during both conditions. No differences in blood flow velocity were found. Although blood pressure was increased and end-expiratory CO2 decreased during the attack, this exerted no influence on blood flow velocity. Neither was a difference in vascular reactivity to voluntary hyperventilation detected between the two conditions. These findings support the notion of functional integrity of the examined large arteries during migraine attacks without aura.
Cephalalgia 1992 Feb
PMID:Blood flow velocities in the vertebrobasilar system during migraine attacks--a transcranial Doppler study. 155 55

Twenty-eight cluster headache patients were examined either in remission (n = 10), in the interparoxysmal period ("cluster phase") (n = 12), or during spontaneously occurring (n = 7), or nitroglycerin provoked (n = 7) attacks. Fourteen healthy controls participated in the study. Oxygen saturation (SaO2), end-tidal CO2 (PCO2), and respiratory rate (R.R.) were recorded for the controls and the patients during the different phases of cluster headache. Both PCO2 and SaO2 tended to be lower during the interparoxysmal period of the cluster phase when compared to the control group or to the remission. During both nitroglycerin-provoked and spontaneous attacks, PCO2 and SaO2 tended to respectively decrease and increase, both when compared with the "cluster phase" and with the period immediately prior to attack ("pre-attack"). Hence the "pre-attack" state may, on an average, be characterized by a slight hypoxia and a slight hyperventilation. Marked, clinically observable hyperventilation was present only in the occasional cluster headache patient. There was no SaO2 decrease from the "cluster phase" (interparoxysmal period) to the period immediately preceding the attack ("pre-attack"), and SaO2 "dips" preceding an attack were only observed in one cluster headache patient. As demonstrated previously by our group, a considerable lowering of SaO2 (i.e. partly to less than or equal to 83%) does only exceptionally lead to attack (Zhao et al, 1990). This observation combined with the evidence presented herein may seem to indicate that the slight pre-attack oxygen desaturation probably is too small to be a symptom-producing factor in cluster headache--be it in the spontaneously occurring or in the induced attack.(ABSTRACT TRUNCATED AT 250 WORDS)
Headache 1992 Mar
PMID:Cluster headache: oxygen saturation and end-tidal CO2 during and without attack. 156 43

Post-polio patients sometimes complain about the occurrence of breathing difficulties decades after the polio infection. We have examined 40 post-polio patients who have had respiratory or non-respiratory poliomyelitis for at least 30 years in an attempt to elucidate whether hypoventilation is common and to what extent certain symptoms and simple lung function tests are related to hypoventilation or incipient hypoventilation. We measured arterial blood gases, vital capacity (VC), maximal expiratory and inspiratory pressures (MEP, MIP) and CO2 rebreathing response. Symptoms were assessed by a yes/no questionnaire. Six patients required respiratory assistance at the onset of the disease. At present, two require nocturnal assisted ventilation. Two patients showed manifest hypoventilation; one of which required night-time ventilator, whereas the other patient had not required ventilatory assistance even at the onset of the disease. Significant correlation (p less than 0.05) was found between arterial carbon dioxide tension (a-PCO2) and VC, MEP and ventilation increase during CO2 rebreathing. A significantly higher a-PCO2 was found among those who required respiratory assistance at the onset of the disease, who admitted headache and who felt the cough ineffective. Low VC and low ventilatory increase during CO2 rebreathing and the presence of headache explained 45% of the variation in a-PCO2 in a multiple regression analysis. We conclude that manifest hypoventilation is rare in this unselected material of post-polio patients and that a vital capacity below 45-50% of predicted normal and the presence of frequent headaches indicate an increased risk to develop hypoventilation.
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PMID:Post-polio lung function. 160 61

We tested the efficacy of nocturnal nasal ventilation (NNV) using the BIPAP ventilator in patients with restrictive thoracic diseases by withdrawing them from NNV for an average of 1 wk. One male and five female patients were enrolled in the study; four with restrictive chest wall diseases, and two with muscular dystrophies. All patients had chronic CO2 retention (PaCO2 greater than 50 mm Hg) and had been improved by using NNV for at least 2 months before the study. Four patients were switched to the BIPAP ventilator from standard portable volume ventilators at least 1 month prior to the study without changes in gas exchange or symptoms. After withdrawal of NNV, patients had no deterioration in daytime vital signs, pulmonary functions, maximal inspiratory or expiratory pressures, or arterial blood gases compared with measures made immediately before withdrawal and 1 wk after resumption. However, patients had more dyspnea at rest, increased daytime somnolence, more morning headaches, less daytime energy, and felt less rested in the morning during withdrawal of NNV. Furthermore, nocturnal monitoring demonstrated greater tachycardia, tachypnea, oxygen desaturation, and hypoventilation during withdrawal of NNV. We conclude that NNV administered by the BIPAP ventilator is effective in ameliorating nocturnal hypoventilation and daytime symptoms in patients with chronic CO2 retention caused by severe restrictive thoracic diseases. These data also suggest that the efficacy of NNV may depend more on amelioration of nocturnal hypoventilation than on resting of ventilatory muscles.
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PMID:Efficacy of nocturnal nasal ventilation in patients with restrictive thoracic disease. 173 43

We measured vascular reactivity--expressed i) as decrease in blood flow velocity (cm/sec) per vol% CO2 decrease due to voluntary hyperventilation and ii) as increase of blood flow velocity during the first minute after resuming normal ventilation, per vol% CO2 increase--in the middle cerebral and basilar artery of 48 migraineurs with attacks without aura, and 17 normal controls. We found no differences for both determinants of vascular reactivity between migraineurs during and outside an attack, and between migraineurs and healthy volunteers. We conclude that the vasomotor reactivity is normal during migraine attacks without aura.
Headache 1991 Oct
PMID:Vascular reactivity during migraine attacks: a transcranial Doppler study. 177 74

Cerebrovascular reactivity to CO2 inhalation was studied by transcranial Doppler sonography in 30 patients with classic or common migraine and 39 healthy controls without clinical or ultrasonic signs of arteriosclerosis. Systolic and diastolic Doppler frequencies of the middle cerebral artery were plotted against end-tidal CO2 partial pressure; the reactivity index (I x R) was defined as relative frequency change during a PCO2 increase of 5 mmHg. In the normal subjects, I x R was 20.0 +/- 6.3 for systolic velocities, and 26.0 +/- 8.2 for diastolic values. Migraineurs during their headache-free interval had significantly higher I x R values on the affected side (mean: 41.6 systolic, 61.2 diastolic), compared with either controls (P less than 0.01) or the contralateral side (mean: 28.3 systolic, 30.8 diastolic; P less than 0.01). During the headache attack, CO2 reactivity was significantly lower than normal only for systolic velocities (mean: 8.3; P less than 0.05). Increased CO2 reactivity is thought to be one phenomenon of migraine. Transcranial Doppler CO2 testing of cerebrovascular reactivity is a reliable method that may be of interest for the diagnostic evaluation and management of migraine patients.
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PMID:Cerebrovascular CO2 reactivity in migraine: assessment by transcranial Doppler ultrasound. 190 49

The effect of voluntary hyperventilation was assessed in 22 cluster headache patients (8 in a cluster period and 14 in a remission) and 19 healthy individuals. Using an ear oximeter and a capnograph with a nasal probe, the oxygen saturation (SaO2) and the end-tidal CO2 were monitored continuously. During the hyperventilation per se, cluster headache patients and controls showed absolute values of end-tidal CO2 and of SaO2 of the same order of magnitude. In the posthyperventilation phase, however, the average of the lowest SaO2 levels was lower in controls than in cluster headache patients. In the posthyperventilation phase, headache patients outside the cluster period showed a trend more similar to that of the controls with respect to SaO2 than did those inside the cluster period. The observed discrepancy might, if reproducible, be a consequence of an altered chemoreceptor sensitivity in cluster headache patients during the bout.
Headache 1991 Mar
PMID:The effect of hyperventilation in cluster headache patients. 207 91


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