PubMed Health⌕ Search

Biomedical subjects

G Hellström

Publications and source records attributed to G Hellström.

At least 19 recordsLinked to original sources
PubMed2001

Ventilation-perfusion inequality and carbon dioxide sensitivity in hypoxaemic chronic obstructive pulmonary disease (COPD) and effects of 6 months of long-term oxygen treatment (LTOT).

UNLABELLED: The aim of our study was to find out how blood gas disturbances in stable, eucapnic, severe chronic obstructive pulmonary disease (COPD) patients with an arterial oxygen tension (PaO(2)) value of 7.7 (6.1-8.4) kPa are affected by ventilation-perfusion (V(A)/Q) relationships and carbon dioxide (CO(2)) sensitivity and how these parameters are influenced by 6 months of long-term oxygen treatment (LTOT). V(A)/Q ratios were measured using the multiple inert gas elimination technique (MIGET). Mouth occlusion pressure 0.1 s after onset of inspiration (Pi0.1) and minute ventilation (V(E)) were measured to assess respiratory drive response (DeltaPi0.1/DeltaPCO(2)) and hypercapnic ventilatory response (HCVR) to CO(2) rebreathing. At the start of LTOT, a normal median respiratory drive response level of 1.2 (0.2-2.3) cm H2O/kPa and a low median HCVR as compared with healthy individuals (P<0.001) were found. However, 7.9 (0-29.8)% of the VE, was directed towards hypoperfused lung areas. The dispersion of ventilation (log SDV; 0.47-1.76), and the dispersion of perfusion (log SDQ; 0.66-1.07) were wider than normal. The PaO(2) level correlated inversely with mean V(A)/Q ratio for ventilation (V mean) and shunt. The PaCO(2) level correlated inversely with HCVR and vital capacity. After 6 months of LTOT, no significant changes in daytime blood gas levels, CO(2)-sensitivity or VA/Q ratios were found. VE tended to be reduced by 1.0 l min-1. CONCLUSIONS: An elevated V mean and probably shunting are important contributing factors for the reduced PaO(2) and hypercapnic ventilatory response is a major determinant of PaCO(2) in eucapnic stable hypoxaemic COPD. Six months of LTOT does not affect blood gases, CO(2) sensitivity or ventilation-perfusion relationships.

Adult↗
PubMed1999

Sleep quality, carbon dioxide responsiveness and hypoxaemic patterns in nocturnal hypoxaemia due to chronic obstructive pulmonary disease (COPD) without daytime hypoxaemia.

In order to clarify whether nocturnal hypoxaemia (arterial oxygen saturation, SaO2 < 90%) may exist in the long-term before daytime hypoxaemia (PaO2 < 8.0 kPa) occurs in chronic obstructive pulmonary disease (COPD), 21 patients with stable severe COPD without daytime hypoxaemia (PaO2 > or = 8.0 kPa) were studied prospectively. Subjects were monitored twice by polysomnography (PSG) 12 months apart. Spirometry was performed, and diffusion capacity (DLCO) and hypercapnic respiratory drive response delta PI0.1 delta PCO2(-1)) were measured during the daytime in conjunction with polysomnography. At the start of the study our subjects had FEV1 %P (FEV1 as a percentage of predicted value) of 26.1 +/- 7.2%, a mean nocturnal nadir SaO2 of 83 +/- 5%, and a mean SaO2 during nocturnal hypoxaemic episodes of 88.0 +/- 0.7%. The patients' delta PI0.1 delta PCO2(-1) was 1.8 +/- 1.4 cm H2O kPa-1 (within the normal range). For the entire study group, no significant change in any lung function or blood gas parameter was noted during the year of observation, and nocturnal SaO2 remained unaltered. Stage I sleep decreased (P < 0.05) after 12 months. Prolonged stage I sleep was associated with nocturnal hypoxaemia at the second PSG. Five subjects developed daytime hypoxaemia and they showed poorer lung function but similar nocturnal hypoxaemia and delta PI0.1 delta PCO2(-1) level compared to the rest of the patients. Patients with sudden SaO2 dips had more pronounced nocturnal hypoxaemia and prolonged wakefulness than 'non-dippers'. In conclusion, the mean level of nocturnal hypoxaemia may persist unaltered for at least 1 yr. COPD patients with exclusively nocturnal hypoxaemia have a hypercapnic drive response within the normal range. Prolonged nocturnal hypoxaemia and reduced whole night oxygenation are associated with increased superficial sleep. Sleep fragmentation and high carbon dioxide sensitivity may be important defence mechanisms against sleep-related hypoxaemia. The appearance of daytime hypoxaemia is preceded by a substantial deterioration in lung function, but by only a minor deterioration of nocturnal hypoxaemia.

Aged↗
PubMed1999

Ketamine antagonises alfentanil-induced hypoventilation in healthy male volunteers.

BACKGROUND: The effects of ketamine on respiration, alone, or in combination with opioids, have not been completely clarified. Both stimulant and depressant effects have been reported, as well as attenuation of opioid-induced hypoventilation at the expense of increased oxygen consumption. These conflicting results might partly be due to dose-dependent mechanisms. We have, therefore, determined the ventilatory effects of ketamine, in combination with alfentanil, using infusions to different pseudo steady-state concentrations. METHODS: On two separate days, eight healthy male volunteers were given alfentanil as a continuous computer-controlled infusion, aiming at a plasma concentration of 50 ng x mL(-1). After reaching apparent steady-state for alfentanil, racemic ketamine or placebo was administered in a protocol randomised for the two days. On the ketamine days a computer-controlled infusion, aiming for escalating ketamine plasma concentrations of 50, 100 and 200 ng x mL(-1), was added to the alfentanil infusion. On the placebo days saline was added. Using a face-mask with an occlusion valve, respiratory parameters were measured during air-breathing and after 6 repetitive 30-s CO2 challenges. RESULTS: The alfentanil infusion induced hypoventilation by decreasing respiratory rate, while tidal volume and respiratory drive were unaffected. This hypoventilation was antagonised by ketamine in a concentration-dependent manner mainly through an increase in respiratory rate. The CO2 response was not affected by alfentanil or ketamine. CONCLUSION: In the dose range of interest for postoperative, intensive-care and pain-clinic settings, ketamine antagonises the resting hypoventilation induced by alfentanil.

Adult↗
PubMed1999

Complications in carotid endarterectomy are predicted by qualifying symptoms and preoperative CT findings.

OBJECTIVES: To relate the 30-day perioperative rate of stroke or death in carotid endarterectomy (CEA) to preoperative qualifying symptoms and to the presence of cerebral infarction (CI) demonstrated on computed tomography (CT). DESIGN: Retrospective clinical study. MATERIAL AND METHODS: Two hundred and seventy-two consecutive CEAs for symptomatic stenosis in 262 patients were analysed. RESULTS: The total complication rate was 5.9%. Patients with retinal symptoms (n = 81) had no complications, TIA patients (n = 76) had 6.6% (p < 0.001). Patients qualifying with minor stroke (n = 113) had complications in 9.7% (N.S. compared to TIA patients). Patients qualifying with cortical symptoms had a significantly higher complication rate compared to those with retinal (8.4% vs. 0%, p = 0.004). The presence of a preoperative CT-verified infarction resulted in a higher risk for stroke or death (9.8% vs 2.8%, p = 0.008). Within the subgroup presenting with minor stroke, the presence of CI resulted in stroke or death in 13.9%. In patients without CI the corresponding figure was 2.4% (p = 0.017). CONCLUSION: The qualifying symptoms and the presence of CI visualized by CT influence the complication rate in CEA. When evaluating risk and comparing outcome, these parameters should be included in reporting standards.

Adult↗
PubMed1996

Carotid artery blood flow and middle cerebral artery blood flow velocity during physical exercise.

Factors controlling cerebral blood flow (CBF) during exercise are complex and incompletely known. Different techniques have shown partly contradictory results of changes in regional and global cerebral perfusion during dynamic exercise in healthy subjects. To elucidate the global CBF response to supine stepwise increasing physical exercise, we measured blood flow in the left common carotid artery (QCCA) and the left internal carotid artery (QICA) simultaneously with the blood flow velocity in the ipsilateral middle cerebral artery (VMCA) using duplex ultrasonography and transcranial Doppler ultrasonography. During moderate exercise intensity (60-67% of maximal capacity), the VMCA increased 14% (P < 0.001), the QICA 17% (P < 0.01), and the QCCA 33% (P < 0.001) compared with baseline values. High physical exercise intensity (80-90% of maximal capacity) tended to reduce VMCA and QICA compared with moderate exercise, in contrast to a continued increase in QCCA. The results indicate an increased global CBF during exercise. This increase was reduced during hard exercise due to a decrease of the arterial PCO2 secondary to hyperventilation.

Adult↗
PubMed1993

Physical exercise increases middle cerebral artery blood flow velocity.

The effect on the middle cerebral artery blood flow velocity (VMCA) of moderate and hard physical exercise on an ergometer cycle was examined in 10 healthy volunteers using transcranial Doppler sonography (TCD). During exercise, the heart rate increased by 136% and the systolic blood pressure by 37% (mean values). During initial moderate exercise, VMCA increased by 51%; in a following period of maximal physical work, VMCA decreased again by 20% in 9 of 10 volunteers although the heart rate continued to increase by 10% and the systolic blood pressure by 5% (mean values). Constriction of the MCA may explain the initial increase of VMCA, suggesting a role for large cerebral arteries in autoregulation. Our data indicate that the subsequent decrease of VMCA is caused by arteriolar constriction, a likely cause of which was hyperventilation during the excessive work period.

Adult↗
PubMed1992

Analgesic administration in children and adults following open heart surgery.

In this study we investigated the administration of analgesics given to patients after open heart surgery (n = 100). The results show that children, especially infants, and elderly patients were given significantly fewer doses of analgesics during the five days after surgery than patients aged greater than 16-70 years. The pattern of pain relief also differed between children and adults, a peak in the number of doses of analgesics occurring on the first day after surgery among children and infants and on the second to third day among adults who continued to get higher numbers of doses than the children up to the fifth day.

Adolescent↗
PubMed1990

Cluster headache and "dynamite headache": blood flow velocities in the middle cerebral artery.

Nitroglycerin (NG) induces in cluster headache patients and controls an increase in systemic diastolic blood pressure and/or heart rate and a decrease in blood flow velocity in the middle cerebral artery (VMCA). Termination of NG induced cluster headache-like attack was correlated to an increase of VMCA compared to the VMCA before NG administration (p less than 0.01). This increase was not found in patients without attack or in controls. The NG induced "dynamite headache" in the controls subsided when blood pressure and heart rate were normalized, but the decrease of VMCA still prevailed. Orbital phlebograms have shown pathologic changes in cluster headache and in Tolosa-Hunt syndrome but not in controls. Ocular sympathetic nerves are involved in cluster headache but seldom in Tolosa-Hunt syndrome. It is suggested that the start of a cluster headache attack is due to an increase and the termination of the attack to a decrease of blood flow to the sympathoplegic phlebopathic cavernous sinus.

Adult↗