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Biomedical subjects

A D ten Harkel

Publications and source records attributed to A D ten Harkel.

14 recordsLinked to original sources

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↗

Circulatory response evoked by a 3 s bout of dynamic leg exercise in humans.

1. The mechanisms underlying the pronounced transient fall in arterial blood pressure evoked by a 3 s bout of bicycle exercise were investigated in twenty healthy young adults and four patients with hypoadrenergic orthostatic hypotension. 2. In healthy subjects a 3 s bout of upright cycling induced a 28 +/- 3 mmHg fall in mean arterial pressure at 12 s. The fall in mean arterial pressure was preceded by a 12 +/- 2 mmHg rise in right atrial pressure at 3 s and accompanied by a 54 +/- 7% increase in left ventricle stroke volume at 6 s. Systemic vascular resistance dropped 48 +/- 2% at 7 s after the start of the manoeuvre to remain at that level for approximately 5 s. The total response lasted about 20 s. During sustained upright cycling the initial fall in mean arterial pressure was also present, but less pronounced (17 +/- 2 vs. 26 +/- 3 mmHg). A 3 s bout of supine cycling in four patients with hypoadrenergic orthostatic hypotension also elicited a pronounced fall in mean arterial pressure (22 +/- 4 mmHg) and in systemic vascular resistance (38 +/- 4%). 3. A bout of exercise with a large muscle mass induces two main effects. First, it mechanically increases filling of the heart due to activation of the muscle pump, resulting in an increase in cardiac output. Second, it induces a drop in systemic vascular resistance. The increase in cardiac output is not sufficient to compensate fully for the pronounced fall in systemic vascular resistance and the result is a transient fall in arterial pressure at the onset of whole-body exercise. The rise in right atrial pressure evoked by 3 s cycling is abrupt and large, but the almost immediate onset and rapid fall of the systemic vascular resistance is too fast for sympathetically mediated reflex effects due to stimulation of the cardiopulmonary afferents. An important factor involved in the drop in systemic vascular resistance appears to be local, non-autonomically mediated vasodilatation in exercising muscles, since it also occurs in patients with autonomic failure.

Adult↗

Differences in circulatory control in normal subjects who faint and who do not faint during orthostatic stress.

We have determined if there are differences in normal subjects who fainted and those who did not faint during prolonged standing. We studied the short-term orthostatic responses in relation to heart rate, blood pressure measured by Finapres, left ventricular stroke volume analysed by pulse contour method, cardiac output and systemic vascular resistance, and also postural blood pressure and heart rate variability as assessed by spectral analysis. Thirteen healthy males without a history of syncope were studied. Three fainted after 10-13 min standing; the ten non-fainters remained upright for 20 min. The initial (first 30 s) postural circulatory adjustment was comparable for blood pressure but the rebound bradycardia was smaller in the fainters (heart rate at 22 s amounted to +13 +/- 10 beats/min above control vs. +1 +/- 5 beats/min in the non-fainters). Upright heart rate at 2 min standing was higher in the fainters (+31 +/- 2 beats/min vs. +20 +/- 5 beats/min), and blood pressure at 7 min standing was lower (-2/+5/+8 +/- 5/5/5 mmHg vs. +11/+13/+16 +/- 10/6/5 mmHg). The responses of stroke volume and cardiac output were comparable but systemic vascular resistance gradually decreased in the fainters from 5 min standing to the onset of fainting (+4 +/- 13% vs. +33 +/- 19% at 7 min standing). In fainters, the variability in upright blood pressure around 0.1 Hz was larger (8.8 mmHg2/Hz for diastolic blood pressure vs. 5.7 +/- 1.5 mmHg2/Hz in non-fainters).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Physical manoeuvres for combating orthostatic dizziness in autonomic failure.

Some patients with orthostatic hypotension combat orthostatic dizziness by leg-crossing and squatting. Changes in blood pressure with these manoeuvres were studied in 7 patients with hypoadrenergic orthostatic hypotension and in 6 healthy subjects. Without leg-crossing, 5 of the patients reported dizziness within 10 min of standing up. Crossing of the legs allowed all to stand for 10 min or more, and there was an associated increase in mean blood pressure of 13 (SD 6) mm Hg compared with 1 (4) in healthy controls; the corresponding figures for squatting were 44 (18) and 8 (6) mm Hg. Patients with orthostatic intolerance should be told about these blood-pressure-raising manoeuvres.

Adult↗

Cardiopulmonary function during 10 days of head-down tilt bedrest.

Pulmonary and cardiovascular responses to simulated weightlessness, i. e. 6 degrees head-down tilt bedrest (HDT) were investigated in six healthy male volunteers (mean age 26 yrs). Pulmonary diffusing capacity, functional residual capacity, pulmonary capillary blood flow, and lung tissue volume were measured by inert gas rebreathing. Heart rate and mean arterial blood pressure were obtained from finger blood pressure readings using a plethysmographic technique (Finapres). The short-term (20 min) response to HDT consisted of a 22% increase in pulmonary blood flow, and 13% and 31% falls in blood pressure and heart rate relative to standing. Functional residual capacity fell by 33%, while lung tissue volume increased insignificantly. Subsequent measurements during 10 days of HDT and 5 days of recovery revealed no further changes in lung volume, lung tissue volume, or blood pressure. However, diffusing capacity fell gradually and remained 4%-5% below baseline values after the 7th day of bedrest and during recovery (p less than 0.05). Pulmonary blood flow decreased by 16% during head-down bedrest and recovered partially within the following 5 days (p less than 0.05). We conclude that during and after simulated weightlessness marked alterations in cardiovascular function and marginal affections of gas exchange can be demonstrated already at rest. They may be considered as contributing factors to orthostatic and exercise intolerance observed after space flight.

Adult↗

Cardiovascular response to lower body negative pressure before, during, and after ten days head-down tilt bedrest.

The haemodynamic response to lower body negative pressure (LBNP) was studied in 6 test subjects before (baseline), during, and after (recovery) ten days of 6 degrees head-down bedrest. The LBNP protocol consisted of a 35 min control period, application of a staircase differential pressure profile (15 min at -15 mmHg; 5 min at -30 mmHg; 15 min at -40 mmHg), and a 10 min post-stress observation period. Cardiac output was measured by a foreign gas rebreathing technique. Finger plethysmographic arterial blood pressure (BP), ECG, and heart rate (HR), lower limb crossectional area, and the electrical impedance of three body segments were recorded continuously. As expected, HDT caused a decrease in plasma volume and total body fluid volume. Resting CO at the end of HDT was 16% below the baseline level and similar to CO in the upright position before HDT. Stroke volume (SV) was also reduced, but there were no significant changes in control HR or BP. Absolute changes in CO and SV during LBNP were similar at baseline and during HDT, but the relative changes were larger during HDT. HR and vasoconstriction responses were enhanced, but presyncope occurred in two subjects. Reduced cardiac filling with decreased stroke volume at rest is the apparent primary cause of the altered LBNP response during HDT.

Adult↗

Influence of posture and prolonged head-down tilt on cardiovascular reflexes.

We investigated the influence of ten days 6 degrees head-down tilt (HDT) on short-term cardiovascular control. To help differentiate between the effects of HDT-induced fluid redistribution and changed autonomic cardiovascular modulation under prolonged HDT, the effect of acute posture changes was investigated as well. Six healthy male volunteers were studied. Continuous finger blood pressure was measured non-invasively by means of Finapres. Heart rate (HR) was derived from the electrocardiogram. Responses to forced breathing (FRSA), Valsalva's manoeuvre (VM), Mental Stress (MS) and Sustained Handgrip (SHG) were measured. Changing posture from HDT to standing enhanced the BP and HR responses to VM, both during straining and after release. During prolonged HDT, responses to VM changed toward the pattern seen in the upright posture before HDT, suggesting a strong influence of fluid redistribution. Neither posture nor prolonged HDT influenced HR variation during FRSA and responses to MS and SHG. BP variation during FRSA was influenced by posture but not by prolonged HDT. Thus, cardiovascular reflex tests which reflect the parasympathetic (FRSA) or the sympathetic (MS and SHG) efferents to the heart were not influenced by posture or prolonged HDT. Only the responses to VM were affected by both posture and prolonged HDT. These results are probably due to a decrease in blood volume and stroke volume under prolonged HDT, an increase in venous distensibility and, to a lesser extent, to inadequate cardiovascular regulatory responses.

Adult↗

Increased orthostatic blood pressure variability after prolonged head-down tilt.

The effect of simulated weightlessness on orthostatic blood pressure regulation was evaluated with passive 70 degrees head-up tilt (HUT) after 10 days 6 degrees head-down tilt (HDT). Six healthy male volunteers were studied. Continuous recording of finger blood pressure (BP) was obtained non-invasively with a FinapresTM device. Instantaneous heart rate (HR) was derived from the electrocardiogram. To quantify orthostatic BP variability, a fast fourier transform (FFT) of the beat-by-beat BP- and RR-interval values was performed. Control HR before HUT after the 10-day HDT period was increased, probably due to an arousal state of the test subjects. The change in BP induced by HUT was not influenced by 10 days' HDT, in contrast to the HR rise which increased from 24 +/- 2 beats/min to 41 +/- 7 beats/min (P less than 0.05). After HDT the total variance in orthostatic BP almost doubled. FFT indicated that this increase in variance can be ascribed to BP oscillations with a frequency of around 0.1 Hz. In three subjects transient HR decelerations during HUT after HDT were observed. Analysis of the relationship between BP and HR in the transients showed that each HR decrease was preceded by a BP increase above normal. These HR decelerations seemed, therefore, to be an effect of the vagal part of the arterial baroreflex and did not necessary signal an impending vasovagal syncope. The present study indicates that although 10 days' HDT do not influence absolute BP responses to 70 degrees HUT BP was maintained by an increased sympathetic activity, reflected by an increased HR response and an augmented variance in BP around 0.1 Hz.

Adult↗

Circulatory autonomic failure 50 years after acute poliomyelitis.

A 59-year old woman who presented with postural dizziness 50 years after an acute episode of poliomyelitis is described. There were no new neurological signs and no evidence of motor neuron disease. She had postural hypotension with an abnormal Valsalva. Investigations led to a diagnosis of hypo-adrenergic orthostatic hypotension, with a predominantly preganglionic sympathetic lesion and intact vagal baroreflex pathways. Although pure autonomic failure and multiple system atrophy are possible causes of circulatory autonomic failure, no other new neurological or autonomic features have developed during a 2 year follow-up. We propose that hypo-adrenergic orthostatic hypotension may be a late complication of poliomyelitis. Deterioration in ambulatory ability in a patient with previous poliomyelitis should additionally include assessment of cardiovascular autonomic function.

Autonomic Nervous System Diseases↗

Spectrum of orthostatic disorders: classification based on an analysis of the short-term circulatory response upon standing.

1. In 31 consecutively referred patients (20 females, 11 males) with overt or suspected orthostatic disorders, the changes in blood pressure and heart rate that occur in the first 2 min of standing were analysed. 2. Blood pressure was measured continuously by Finapres. The blood pressure and heart rate responses after 1-2 min of standing (early steady-state response) were used to classify the patients as follows: group I (n = 17, age 42 +/- 17 years), normal early steady-state blood pressure and heart rate responses; group II (n = 5, age 40 +/- 14 years), combination of normal early steady-state blood pressure and postural tachycardia; group III (n = 9, age 51 +/- 14 years), hypotensive orthostatic response with (4/9) or without (5/9) postural tachycardia. We examined whether additional information could be obtained by beat-to-beat analysis of the initial circulatory response (first 30 s). It was quantified by identifying the blood pressure trough and overshoot and the maximum heart rate and relative bradycardia. 3. The initial drop in systolic and diastolic blood pressures did not differ between the three groups. A recovery of blood pressure with a systolic and/or diastolic blood pressure overshoot was present in all group I and II patients, but was absent in all except two patients in group III. The initial maximum heart rate increase did not differ between the three groups. The relative bradycardia was less in groups II and III than in group I. 4. We conclude that analysis of the beat-to-beat blood pressure changes in the first 30 s after the onset of standing provides almost all the information that is necessary to determine abnormalities in orthostatic circulatory control.

Adolescent↗

Contrasting effects of acute and chronic volume expansion on orthostatic blood pressure control in a patient with autonomic circulatory failure.

We studied the effects of acute and chronic volume expansion on orthostatic blood pressure control in a 22-year-old female with hypoadrenergic orthostatic hypotension. Acute volume expansion on two occasions had unexpected effects: a decrease respectively no change in orthostatic tolerance and no change in upright blood pressure immediately after volume expansion followed by a marked improvement 8 h thereafter. The time course of changes in haematocrit and serum protein indicated an initial extravasation of plasma followed by a subsequent larger fluid shift back to the intravascular space. These effects had vanished after 3 days. Chronic volume expansion by head-up tilt at night and fludrocortisone resulted in a marked improvement in orthostatic blood pressure control at a comparable increment in body weight and sodium balance for the next 7 years until now. The circadian circulatory variation with orthostatic blood pressure lowest in the morning remained present after chronic volume expansion. We conclude in this patient that the effects of acute volume expansion on orthostatic blood pressure in autonomic failure are complex and not predictive for the beneficial effects of chronic volume expansion.

Adult↗

Cardiovascular response to coughing: its value in the assessment of autonomic nervous control.

1. The relationship between blood pressure and heart rate responses to coughing was investigated in 10 healthy subjects in three body positions and compared with the circulatory responses to commonly used autonomic function tests: forced breathing, standing up and the Valsalva manoeuvre. 2. We observed a concomitant intra-cough increase in supine heart rate and blood pressure and a sustained post-cough elevation of heart rate in the absence of arterial hypotension. These findings indicate that the sustained increase in heart rate in response to coughing is not caused by arterial hypotension and that these heart rate changes are not under arterial baroreflex control. 3. The maximal change in heart rate in response to coughing (28 +/- 8 beats/min) was comparable with the response to forced breathing (29 +/- 9 beats/min, P greater than 0.4), with a reasonable correlation (r = 0.67, P less than 0.05), and smaller than the change in response to standing up (41 +/- 9 beats/min, P less than 0.01) and to the Valsalva manoeuvre (39 +/- 13 beats/min, P less than 0.01). 4. Quantifying the initial heart rate response to coughing offers no advantage in measuring cardiac acceleratory capacity; standing up and the Valsalva manoeuvre are superior to coughing in evaluating arterial baroreflex cardiovascular function.

Adult↗