A. D. J. Ten Harkel

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.

Treatment of orthostatic hypotension with sleeping in the head-up tilt position, alone and in combination with fludrocortisone

We studied the effect of sleeping in the head‐up tilt (HUT) position, alone and in combination with fludrocortisone, on orthostatic tolerance and blood pressure (BP) in six patients with hypoadrenergic orthostatic hypotension. A high salt diet of 150–200 mmol Na+ d−1 was also administered. Combined treatment reduced orthostatic dizziness in all patients (P < 0.001), and increased the maximal standing period to at least 10 min. HUT alone (n = 4) reduced the BP decrease after 1 min of standing from −64/‐42/‐25 ± 29/21/17mmHg to −53/‐37/‐23 ± 31/24/20 mmHg (P < 0.01 for systolic BP). Addition of fludrocortisone to HUT (HUT/fludro) (n = 5) further reduced the BP decrease after 1 min of standing from −63/ −40/ −24 ± 20/12/11 mmHg to −21/‐19/‐8 ± 12/10/5 mmHg (P < 0.05 for systolic, mean and diastolic BP, respectively). BP at maximal standing time increased from 58/47/42 ± 9/8/7 mmHg initially to 95/69/57 ± 27/22/20 mmHg during combined treatment (P < 0.05 for systolic and mean BP), and remained unchanged during the 14‐month (range 8–70 month) follow‐up period. Nocturnal sodium excretion decreased from 8.0 ± 2.3 mmol h−1 to 5.9 ± 1.9 mmol h−1 with combined treatment; body weight increased by 1.6 kg on average (range 0.5‐2.4 kg) (P < 0.01). We conclude that the combination of HUT and fludrocortisone effectively minimizes orthostatic symptoms and increases orthostatic BP in patients with hypo‐adrenergic orthostatic hypotension.

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.

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).In conclusion, the circulatory adjustments to active standing in fainters is different from non-fainters, as they lose vasoconstrictor tone after 5 min of standing despite an increase in blood pressure variability and heart rate which suggest increased sympathetic activity. Whether there are other opposing factors, which include vasodilator substances, is discussed.

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 hypoadrenergic 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.