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Biomedical subjects

W Wieling

Publications and source records attributed to W Wieling.

At least 19 recordsLinked to original sources
PubMed2003

[A patient with an unexplained loss of consciousness: a case for the neurologist or the cardiologist?].

Three patients, a woman aged 62 and two men aged 22 and 77 years respectively, were admitted because of an unexplained loss of consciousness. In the woman and younger man these complaints were caused by a vasovagal reaction, and in the older man by hypersensitivity of the carotid sinus. In a hospital setting, the examination of patients with a loss of consciousness often leads to discussions between the neurologist and the cardiologist. Elaborate additional testing seldom reveals epilepsy or cardiac arrhythmia as the cause. A thorough medical history can exclude both diagnoses in almost all cases. Physicians should be aware that most patients experience a vasovagal syncope and that this might be triggered by very common circumstances. Knowledge of these triggers and the epidemiology of loss of consciousness might prevent the patients from being examined by different specialists and undergoing unnecessary additional tests.

Adult↗
PubMed2003

[Initial diagnostic strategy in the case of transient losses of consciousness: the importance of the medical history].

It is estimated that almost half of the people experience a transient loss of consciousness at some time during their life. In young patients (< 35 years) the cause is mostly a reflex syncope. In older patients the common causes are orthostatic and postprandial hypotension, sinus caroticus syndrome, cardiac arrhythmias and valvular disorders. The medical history can identify a probable cause of the transient loss of consciousness in almost all young patients (< 35 years) and in the majority of older patients. A physical examination and an ECG should be performed in all patients who have experienced a transient loss of consciousness, other than those with classical vasovagal syncope, in order to exclude orthostatic hypotension and dangerous cardiac causes.

Adult↗
PubMed2003

Pilots with vasovagal syncope: fit to fly?

Two pilots who had experienced vasovagal syncope were grounded by the aeromedical service. Pilot A had experienced three episodes of syncope in medical settings, none during flight. Pilot B had experienced four episodes of syncope in emotional/medical settings, one during flight. Whether a pilot who experienced one or more episodes of vasovagal syncope is declared fit to fly now depends on the number of episodes experienced. We propose that pilots should be assessed individually. Certainty of the diagnosis of vasovagal syncope, the chance and predictability of recurrences during flight, and the possibility of effective therapy should be assessed. Chance of recurrence during flight is low when the triggering factor is known and avoidable. Pilots with syncopal episodes in predictable (e.g., medical) situations, with clear prodromal symptoms and/or effective therapy, should be declared fit to fly. A symptom-free period and/or restriction to fly 'as or with a co-pilot' can be considered.

Adult↗
PubMed2002

Hemodynamic and neurohumoral responses to head-up tilt in patients with chronic fatigue syndrome.

BACKGROUND: Data on the prevalence of orthostatic intolerance (OI) in patients with chronic fatigue syndrome (CFS) are limited and controversial. We tested the hypothesis that a majority of CFS patients exhibit OI during head-up tilt. METHODS: Hemodynamic and neurohumoral responses to 40 minutes of head-up tilt were studied in 36 CFS patients and 36 healthy controls. Changes in stroke volume, cardiac output and peripheral vascular resistance were estimated from finger arterial pressure waveform analysis (Modelflow). Blood samples were drawn before and at the end of head-up tilt for measurement of plasma catecholamines. RESULTS: At baseline, supine heart rate was higher in CFS patients (CFS: 66.4 +/- 8.4 bpm; controls: 57.4 +/- 6.6 bpm; p < 0.001) as was the plasma epinephrine level (CFS: 0.11 +/- 0.07 nmol/l; controls: 0.08 +/- 0.07 nmol/l: p = 0.015). An abnormal blood pressure and/or heart rate response to head-up tilt was seen in 10 (27.8 %) CFS patients (6 presyncope, 2 postural tachycardia, 2 tachycardia and presyncope) and 6 (16.7 %, p = 0.26) controls (5 presyncope, 1 tachycardia, 2 tachycardia and presyncope). Head-up tilt-negative CFS patients showed a larger decrease in stroke volume during tilt (-46.9 +/- 10.6) than head-up tilt-negative controls (-40.3 +/- 13.6 %, p = 0.008). Plasma catecholamine responses to head-up tilt did not differ between these groups. CONCLUSION: Head-up tilt evokes postural tachycardia or (pre)syncope in a minority of CFS patients. The observations in head-up tilt-negative CFS patients of a higher heart rate at baseline together with a marked decrease in stroke volume in response to head-up tilt may point to deconditioning.

Adult↗
PubMed2002

The fainting lark.

Explore the source record for details and available documents.

Cerebrovascular Circulation↗
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↗