14 research outputs found
Cerebral haemodynamics in man : clinical and applied observations
EThOS - Electronic Theses Online ServiceGBUnited Kingdo
Effect of sildenafil and acclimatization on cerebral oxygenation at altitude
Phosphodiesterase-5 inhibitors decrease hypoxic pulmonary vasoconstriction under hypobaric hypoxia, but are not known to affect cerebral blood flow or oxygenation. The present study was designed to evaluate the effect of sildenafil on cerebral haemodynamics during acute exposure to altitude and after acclimatization. Ten subjects were studied 1 and 3 days after rapid ascent to 3480 m before and for two consecutive hours after taking sildenafil (50 mg). Before acclimatization, HR (heart rate) rose at 1 h (76.3+/-1.0 beats/min compared with 72.5+/-1.5 beats/min at baseline; P0.05). Mean BP (blood pressure) fell from 96.0+/-2.0 mmHg at baseline to 91.7+/-2.5 (P<0.001) at 1 h and 89.8+/-1.8 mmHg (P<0.0001) at 2 h, whereas SaO2 (arterial oxygen saturation) increased from 83.9+/-0.5% at baseline to 85.3+/-0.4% (P<0.0001) at 1 h and 85.0+/-0.5% (P<0.01) at 2 h. MCAV [MCA (middle cerebral artery) velocity] and PETCO2 (end-tidal partial pressure of CO2) were unchanged, but rSO2 (regional cerebral oxygen saturation) rose progressively at 1 h (62.7+/-0.8%; P<0.05) and 2 h (65.3+/-0.9%; P<0.0001) compared with baseline (59.3+/-1.3%). After 3 days of acclimatization, resting rSO2 and RMCA (MCA resistance) increased and oxygen delivery fell. Changes in HR and mean BP after sildenafil were similar to day 1, but SaO2 did not change. However, rSO2 increased [61.7+/-0.9% at baseline to 65.0+/-1.0% (P<0.0001) at 1 h and 64.0+/-0.9% (P<0.001) at 2 h], despite a reduction in MCAV [65.3+/-1.8 cm/s at baseline to 61.3+/-1.5 cm/s (P<0.01) at 1 h and 60.9+/-1.7 cm/s (P<0.0001) at 2 h] and PETCO2 [4.1+/-0.05 kPa at baseline to 4.0+/-0.04 kPa at 2 h (P<0.01)]. These observations suggest that sildenafil improves cerebral oxygenation at altitude. Whereas the early changes before acclimatization may be largely pulmonary in origin, the later observations may be a direct cerebral effect which warrants further study
The association between early neurological deterioration and whole blood purine concentration during acute stroke
Background
Early neurological deterioration (END) is common after stroke. Prediction could identify patients requiring additional monitoring and intervention. Purines, breakdown products of adenosine triphosphate which accumulate during acute hypoxia, may reflect the subclinical presence of vulnerable tissue. We considered whether whole blood purine concentration (WBPC) measurements during acute stroke were associated with subsequent END.
Methods
Patients within 4.5 h of stroke onset underwent point-of-care finger-prick measurement of WBPC and blinded assessment of symptom severity using the National Institutes of Health Stroke Scale (NIHSS). END was defined as an NIHSS increase ≥2 points at 24–36 h compared to baseline.
Results
15/152 (9.8%) patients experienced END with a median [IQR] NIHSS increase of 4 [2–7] points. There were no strong associations between END and baseline NIHSS, clinical stroke subtype, thrombolytic therapy, physiological characteristics or time to assay. The median [IQR] WBPC concentration (uM) was higher before the occurrence of END but without statistical significance (7.21 [4.77–10.65] versus 4.83 [3.00–9.02]; p = 0.1). Above a WBPC threshold of 6.05uM, the risk of END was significantly greater (odds ratio 3.7 (95% CI 1.1–12.4); p = 0.03).
Conclusion
Although the study lacked statistical power, early WBPC measurement could be a convenient biomarker for identifying acute stroke patients at risk of END, but further evaluation is required
Cerebral artery dilatation maintains cerebral oxygenation at extreme altitude and in acute hypoxia : an ultrasound and MRI study
Transcranial Doppler is a widely used noninvasive technique for assessing cerebral artery blood flow. All previous high altitude studies assessing cerebral blood flow (CBF) in the field that have used Doppler to measure arterial blood velocity have assumed vessel diameter to not alter. Here, we report two studies that demonstrate this is not the case. First, we report the highest recorded study of CBF (7,950 m on Everest) and demonstrate that above 5,300 m, middle cerebral artery (MCA) diameter increases (n=24 at 5,300 m, 14 at 6,400 m, and 5 at 7,950 m). Mean MCA diameter at sea level was 5.30 mm, at 5,300 m was 5.23 mm, at 6,400 m was 6.66 mm, and at 7,950 m was 9.34 mm (P<0.001 for change between 5,300 and 7,950 m). The dilatation at 7,950 m reversed with oxygen. Second, we confirm this dilatation by demonstrating the same effect (and correlating it with ultrasound) during hypoxia (FiO2=12% for 3 hours) in a 3-T magnetic resonance imaging study at sea level (n=7). From these results, we conclude that it cannot be assumed that cerebral artery diameter is constant, especially during alterations of inspired oxygen partial pressure, and that transcranial 2D ultrasound is a technique that can be used at the bedside or in the remote setting to assess MCA caliber
Registry report on prediction by Pocock cardiovascular score of cerebral microemboli acutely following carotid endarterectomy.
Background: Cerebral microemboli may lead to ischaemic neurological complications after carotid endarterectomy (CEA). The association between classical cardiovascular risk factors and acute cerebral microemboli following carotid surgery has not been studied. The aim of this study was to explore whether an established cardiovascular risk score (Pocock score) predicts the presence of cerebral microemboli acutely after CEA. Subjects and methods: Pocock scores were assessed for the 670 patients from the Carotid Surgery Registry (age 71±1 (SEM) years, 474 (71%) male, 652 (97%) Caucasian) managed from January 2002 to December 2012 in the Regional Vascular Centre at University Hospitals Coventry and Warwickshire NHS Trust, which serves a population of 950 000. CEA was undertaken in 474 (71%) patients for symptomatic carotid stenosis and in 196 (25%) asymptomatic patients during the same period. 74% of patients were hypertensive, 71% were smokers and 49% had hypercholesterolaemia. Results: A high Pocock score (≥2.3%) was significantly associated with evidence of cerebral microemboli acutely following CEA (P=0.039, Mann-Whitney (MW) test). A Pocock score (≥2.3%) did not predict patients who required additional antiplatelet therapy (microemboli signal (MES) rate >50 hour-1: P=0.164, MW test). Receiver operating characteristic analysis also showed that the Pocock score predicts acute postoperative microemboli (area under the curve (AUC) 0.546, 95% CI 0.502 to 0.590, P=0.039) but not a high rate of postoperative microemboli (MES >50 hour-1: AUC 0.546, 95% CI 0.482 to 0.610, P=0.164). A Pocock score ≥2.3% showed a sensitivity of 74% for the presence of acute postoperative cerebral microemboli. A Pocock score ≥2.3% also showed a sensitivity of 77% and a negative predictive value of 90% for patients who developed a high microembolic rate >50 hour-1 after carotid surgery. Conclusion: These findings demonstrate that the Pocock score could be used as a clinical tool to identify patients at high risk of developing acute postoperative microemboli
Carbon dioxide contributes to the beneficial effect of pressurization in a portable hyperbaric chamber at high altitude
Effect of exercise on cerebral perfusion in humans at high altitude
The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable, recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m, mean (SD) cerebral oxygenation (rSO2%) increased during submaximal exercise from 68.4 (SD 2.1) to 70.9 (SD 3.8) (P < 0.0001) and at maximal oxygen uptake (V̇O2 max) to 69.8 (SD 3.1) (P < 0.02). In contrast, at each of the high altitudes studied, rSO2 was reduced during submaximal exercise from 66.2 (SD 2.5) to 62.6 (SD 2.1) at 3,610 m (P < 0.0001), 63.0 (SD 2.1) to 58.9 (SD 2.1) at 4,750 m (P < 0.0001), and 62.4 (SD 3.6) to 61.2 (SD 3.9) at 5,260 m (P < 0.01), and at V̇O2 max to 61.2 (SD 3.3) at 3,610 m (P < 0.0001), to 59.4 (SD 2.6) at 4,750 m (P < 0.0001), and to 58.0 (SD 3.0) at 5,260 m (P < 0.0001). Cerebrovascular resistance tended to fall during submaximal exercise (P = not significant) and rise at V̇O2 max, following the changes in arterial oxygen saturation and end-tidal CO2. Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at V̇O2 max, but at high altitude peaked at 30% of V̇O2 max and then fell progressively at higher levels of exercise. The fall in rSO2 and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and high-altitude cerebral edema
Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite: 2014 update.
The Wilderness Medical Society convened an expert panel to develop a set of evidence-based guidelines for the prevention and treatment of frostbite. We present a review of pertinent pathophysiology. We then discuss primary and secondary prevention measures and therapeutic management. Recommendations are made regarding each treatment and its role in management. These recommendations are graded on the basis of the quality of supporting evidence and balance between the benefits and risks or burdens for each modality according to methodology stipulated by the American College of Chest Physicians. This is an updated version of the original guidelines published in Wilderness & Environmental Medicine 2011;22(2):156-166