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Biomedical subjects

W Wieling

Publications and source records attributed to W Wieling.

At least 19 recordsLinked to original sources
PubMed2001

[Labile hypertension due to iatrogenic denervation of the carotid sinus].

Two patients, a man and a woman aged 36 and 40 years, respectively, were found to have disturbed blood pressure regulation after medical intervention in the jugular area. The man had undergone radiation therapy of the neck due to regional lymph node involvement of a nasopharyngeal carcinoma. Six years later he developed episodic complaints of headache accompanied by labile hypo- and hypertension. Mental and physical stimuli resulted in excessive sympathetic activation. In the woman, a carotid body tumour was resected bilaterally. There was an immediate onset of hypertension after surgery. In both patients, the clinical syndrome was attributed to afferent baroreflex failure due to carotid sinus denervation.

Adult↗
PubMed2001

Initial orthostatic hypotension as a cause of recurrent syncope: a case report.

A 60-year-old male patient with recurrent unexplained syncope on standing was studied. During continuous, noninvasive blood pressure (BP) recording with a Finapres device, an abnormally large and symptomatic initial decrease in systemic BP was documented. After 2 minutes of standing, BP had recovered. The transient decrease in BP was attributed to the use of a combination of antidepressants known to interfere with sympathetic function. This case shows the importance of continuous, noninvasive BP measurement on standing: routine intermittent BP recording would have missed the abnormality. In patients using medications such as antidepressants, initial transient hypotension should be considered as the cause of falls and syncope.

Antidepressive Agents↗
PubMed2001

Psychological treatment of malignant vasovagal syncope due to bloodphobia.

A 17-year-old boy with frequent faints due to blood-injury phobia was studied. During cardiovascular reflex investigation in our syncope unit, 50 seconds of asystole were recorded. He was treated using systematic desensitization with muscular tension and cognitive techniques by the Pediatric Psychosocial Department and has not experienced syncopal events again.

Adolescent↗
PubMed2001

Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients.

OBJECTIVE: Total peripheral vascular resistance (TPR) decreases in thyrotoxicosis and increases in hypothyroidism. Several mechanisms may be involved, including adaptation to changes in heat production and direct non-genomic effects of tri-iodothyronine (T3) on vascular smooth muscle cells. The aim of this study was to see if changes in TPR are related to changes in plasma concentrations of the endothelial hormones adrenomedullin and endothelin-1 as well as other hormones affecting vasculature. DESIGN: A prospective study. SUBJECTS: Eleven hypothyroid patients (pretreatment: thyroid-stimulating hormone (TSH) 68 (38-201) mU/l, T3 0.7 (0.35-1.5) nmol/l, fT4 3.0 (2.0-5.9) pmol/l, median (range)) and 14 with hyperthyroidism (pretreatment: TSH 0.02 (<0.01-0.06) mU/l, T3 6.4 (2.3-13.0) nmol/l, fT4 56.1 (22.9-70.0) pmol/l) were studied before treatment and 3 months after reaching the euthyroid state. Blood collection was carried out simultaneously with the recording of finger arterial pressure (FINAP). Cardiac output and TPR were derived from stroke volume computations by modelling flow from the FINAP signal. RESULTS: Thyroid-function tests of hypothyroid and thyrotoxic patients did not differ after restoration of the euthyroid state. TPR, expressed in arbitrary units (AU), decreased after correction of hypothyroidism (from 1.32+/-0.65 to 0.96+/-0.36 AU, P=0.04) and increased after correction of hyperthyroidism (from 0.75+/-0.18 to 1.10+/-0.35 AU, P=0.007). Adrenomedullin concentrations did not change during the transition from the hypothyroid state 3.2(0.9-11.0) pmol/l to the euthyroid state 4.9(0.9-8.6) pmol/l, but decreased after treatment of hyperthyroidism, from 5.2(0.9-11.0) pmol/l to 2.2(0.9-5.4) pmol/l. Plasma endothelin-1 was undetectable in all samples. Changes in TPR upon treatment correlated with log DeltafT4 (r=-0.65, P=0.001), log DeltaT3, (r=-0.57, P=0.006), Delta noradrenaline (r=0.54, P=0.02) and Delta ANP (atrial natriuretic peptide) (r=-0.59, P=0.004). Multiple linear regression analysis indicated that only T3 was an independent determinant of TPR. Changes in T3 accounted for 46% of the variability in the changes in TPR. CONCLUSIONS: TPR is reduced in thyrotoxicosis and increased in hypothyroidism. Restoration of the euthyroid state normalizes TPR. Changes in TPR are not related to plasma adrenomedullin concentrations, but 46% could be explained by changes in T3. Altered ANP secretion and adrenergic tone may contribute to the T3-induced changes in TPR.

Adrenomedullin↗
PubMed2001

Mechanisms underlying the impairment in orthostatic tolerance after nocturnal recumbency in patients with autonomic failure.

In the present study, we have assessed in patients with neurogenic orthostatic hypotension the haemodynamics underlying the reduced tolerance to standing after prolonged recumbency at night. In 10 patients with neurogenic orthostatic hypotension (age 33-68 years), of which seven were being treated with fludrocortisone and/or sleeping in the 12 degrees head-up tilt position, 24 h continuous non-invasive finger blood pressure was recorded by a Portapres device. Beat-to-beat blood pressure, heart rate, stroke volume, cardiac output and total peripheral vascular resistance obtained by pulse contour analysis were assessed during 5 min of standing in the evening (at 22.30 hours) and in the morning (at 06.30 hours). On average, the inverse of the normal 24 h blood pressure profile was found, with a large diversity in blood pressure profiles among patients. Supine blood pressure values were similar, but standing blood pressure values were lower in the morning than in the evening (P<0.01). This resulted from larger falls in stroke volume and cardiac output upon standing in the morning compared with the evening, while total peripheral resistance did not change. There was no relationship between the decrease in body weight during the night (mean 0.9 kg; range 0.2-1.6 kg) and the evening-morning difference in standing blood pressure. We conclude that, in patients with neurogenic orthostatic hypotension, the impaired tolerance to standing in the morning is due to larger falls in stroke volume and cardiac output. Not only nocturnal polyuria, but also a redistribution of body fluid, are likely mechanisms underlying the pronounced decreases in stroke volume and cardiac output after prolonged recumbency at night.

Adult↗
PubMed2000

[Three patients with unrecognized orthostatic intolerance].

Three patients, men aged 20, 50 and 56 suffered from orthostatic intolerance and syncope for years, despite visits to many doctors. Medical history and cardiovascular reflex investigation revealed problems with the orthostatic blood pressure regulation, caused by initial orthostatic dysregulation, vasovagal syncope and pure autonomic failure, respectively. A structured medical history as well as blood pressure measurements in the supine and standing positions can reveal the diagnosis in many instances of syncope. After confirming the diagnosis, the first concern is a clear explanation of the underlying problems to the patient. Treatment with volume expansion should be considered.

Adult↗
PubMed2000

Fludrocortisone and sleeping in the head-up position limit the postural decrease in cardiac output in autonomic failure.

Treatment with head-up tilt sleeping and low-dose fludrocortisone effectively minimizes orthostatic symptoms and increases orthostatic blood pressure in patients with neurogenic orthostatic hypotension. The aim of the present study was to examine whether the improvement in orthostatic blood pressure during combined treatment with low-dose fludrocortisone and nocturnal head-up tilt in patients with neurogenic orthostatic hypotension can be attributed to expansion of plasma volume or to increased total peripheral resistance. The effects of a 3-week treatment with fludrocortisone and nocturnal head-up tilting on the postural changes in arterial pressure, heart rate, and cardiac output (pulse contour) were evaluated in eight consecutive patients with orthostatic hypotension. The period during which the patients were able to remain in the standing position without orthostatic complaints increased minimally from 3 to 10 minutes. The decrease in arterial pressure after 1 minute of standing--(means with standard deviations in parentheses) systolic, 49 (20) mm Hg; diastolic, 18 (11) mm Hg--before treatment was produced by a greater than normal decrease in cardiac output: 37% (10%) in patients with neurogenic orthostatic hypotension versus -14% (8%) in control subjects. Treatment increased upright arterial pressure from 83 (19) mm Hg systolic and 55 (13) mm Hg diastolic to 114 (22) mm Hg systolic and 60 (16) mm Hg diastolic by limiting the decrease in cardiac output. Body weight increased but hematocrit did not change. Leg pressure-volume relationship decreased in the two patients studied. The responses of plasma renin activity and aldosterone to orthostatic stress prior to treatment were subnormal and became even lower after treatment. The improvement in upright blood pressure in orthostatic hypotension during treatment with fludrocortisone and nocturnal head-up sleeping is the result of a reduction in the orthostatic decrease in cardiac output. Preliminary data suggest that the expanded body fluid volume is allocated to the perivascular space rather than to the intravascular space.

Adult↗
PubMed2000

Treatment of vasovagal syncope: pacemaker or crossing legs?

A 50-year-old male patient continued to experience syncope after implantation of a pacemaker. During cardiovascular examination, the patient showed a typical vasovagal response, with normal pacemaker function. Leg crossing, which prohibits the pooling of blood in the legs and abdomen, at the onset of symptoms helped to prevent this response. The authors recommend a course of leg crossing as a measure to treat vasovagal syncope.

Abdomen↗
PubMed2000

Orthostatic tolerance, cerebral oxygenation, and blood velocity in humans with sympathetic failure.

BACKGROUND AND PURPOSE: Patients with orthostatic hypotension due to sympathetic failure become symptomatic when standing, although their capability to maintain cerebral blood flow is reported to be preserved. We tested the hypothesis that in patients with sympathetic failure, orthostatic symptoms reflect reduced cerebral perfusion with insufficient oxygen supply. METHODS: This study addressed the relationship between orthostatic tolerance, mean cerebral artery blood velocity (V(mean), determined by transcranial Doppler ultrasonography), oxygenation (oxyhemoglobin [O(2)Hb], determined by near-infrared spectroscopy), and mean arterial pressure at brain level (MAP(MCA), determined by finger arterial pressure monitoring [Finapres]) in 9 patients (aged 37 to 70 years; 4 women) and their age- and sex-matched controls during 5 minutes of standing. RESULTS: Supine MAP(MCA) (108+/-14 versus 86+/-14 mm Hg) and V(mean) (84+/-21 versus 62+/-13 cm. s(-1)) were higher in the patients. After 5 minutes of standing, MAP(MCA) was lower in the patients (31+/-14 versus 72+/-14 mm Hg), as was V(mean) (51+/-8 versus 59+/-9 cm. s(-1)), with a larger reduction in O(2)Hb (-11. 6+/-4 versus -6.7+/-4.5 micromol. L(-1)). Four patients terminated standing after 1 to 3.5 minutes. In these symptomatic patients, the orthostatic fall in V(mean) was greater (45+/-6 versus 64+/-10 cm. s(-1)), and the orthostatic decrease in O(2)Hb (-12.0+/-3.3 versus -7.6+/-3.9 micromol. L(-1)) tended to be larger. The reduction in MAP(MCA) was larger after 10 seconds of standing, and MAP(MCA) was lower after 1 minute (25+/-8 versus 40+/-6 mm Hg). CONCLUSIONS: In patients with sympathetic failure, the orthostatic reduction in cerebral blood velocity and oxygenation is larger. Patients who become symptomatic within 5 minutes of standing are characterized by a pronounced orthostatic fall in blood pressure, cerebral blood velocity, and oxygenation manifest within the first 10 seconds of standing.

Adult↗
PubMed1999

[Physical diagnosis--paradoxical pulse].

Pulsus paradoxus is generally defined as a decline in the systemic systolic blood pressure by more than 10 mmHg during inspiration. The main clinical situations in which a paradoxical pulse may be observed are inflow obstruction into the heart (as in exsudative pericarditis or cardiac tamponade) or extreme respiratory variations in intrathoracal pressure (as during an asthma attack). However, clinical studies indicate that in both situations the predictive value of a present or absent pulsus paradoxus is rather limited.

Airway Obstruction↗
PubMed1999

Pathophysiological basis of orthostatic hypotension in autonomic failure.

In patients with autonomic failure orthostatic hypotension results from an impaired capacity to increase vascular resistance during standing. This fundamental defect leads to increased downward pooling of venous blood and a consequent reduction in stroke volume and cardiac output that exaggerates the orthostatic fall in blood pressure. The location of excessive venous blood pooling has not been established so far, but present data suggest that the abdominal compartment and perhaps leg skin vasculature are the most likely candidates. To improve the orthostatic tolerance in patients with autonomic failure, protective measures that reduce excessive orthostatic blood pooling have been developed and evaluated. These measures include physical counter-manoeuvres and abdominal compression.

Autonomic Nervous System Diseases↗
PubMed1999

Baroreflex failure following radiation therapy for nasopharyngeal carcinoma.

The authors present a 51-year-old man with right-sided nasopharyngeal carcinoma who was treated for regional lymph node involvement by bilateral radiation therapy of the neck. Six years later he presented with episodic complaints of headache, flushing, and palpitations accompanied by elevations of blood pressure. Examination of arterial baroreflex function indicated selective afferent carotid sinus denervation. Cross spectral analysis of spontaneous heart rate and blood pressure variability showed decreased arterial baroreflex sensitivity (6.5 ms/mm Hg). Twenty-four hour measurements of blood pressure and heart rate variability showed labile hypertension during normal daytime activities. Baroreflex failure in this patient probably represents a late complication of bilateral radiation therapy of the neck.

Adult↗
PubMed1999

Patients' choice of portable folding chairs to reduce symptoms of orthostatic hypotension.

Patients with neurogenic orthostatic hypotension may use portable folding chairs to prevent or reduce symptoms of low blood pressure. However, a concomitant movement disorder may limit the use of these chairs in daily living. In this prospective study, 13 patients with orthostatic hypotension, balance disturbance associated with motor disability, or both examined three commercially available portable folding chairs. A questionnaire was used to document the characteristics in chair design that were relevant for satisfactory use to these patients. Armrests, seat width, and an adjustable sitting height were found to be important features of a portable folding chair. One chair was selected by 11 of 13 patients to fit most needs.

Aged↗
PubMed1998

[No strong evidence of disturbed regulation of blood pressure in chronic fatigue syndrome].

Recent medical publications postulate a connection between the Chronic Fatigue Syndrome (CFS) and disturbed regulation of the circulation, manifesting itself during orthostatic stress testing. Four studies were published on the circulatory response on prolonged head up tilt testing. Numerous CFS patients displayed postural tachycardia or syncope during the test. However, many CFS patients examined had had orthostatic symptoms prior to the examination. It is not certain that cardiovascular dysregulation is present in CFS patients without orthostatic symptoms. It is also not clear whether such a dysregulation would be the effect of physical inactivity or a manifestation of a subtle form of autonomic neuropathy.

Adolescent↗