Journal: J Pediatr 2002 Apr;140(4):387-9
Author: Rowe PC.
Affiliation: Divsion of Pediatrics and Adolescent Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
NLM Citation: PMID: 12006948
Chronic fatigue is a prominent symptom in a variety of overlapping syndromes of circulatory dysfunction, the most notable examples of which are neurally mediated hypotension (NMH) and postural tachycardia syndrome (POTS). An early suggestion that such abnormalities were treatable causes of symptoms in what we now call chronic fatigue syndrome (CFS) was made in 1940 by Alexander MacLean and Edgar Allen.1
They described a group of patients who experienced excessive acceleration of the heart and hypotension after moving from the recumbent to the erect posture, usually associated with symptoms of orthostatic exhaustion, blurring of vision, weakness on exercise, and syncopal episodes. McLean and Allen attributed the tachycardia to a reduced venous return to the heart, in part because symptoms and hemodynamic changes could be provoked within 10 seconds by Flack’s test, which involved forced expiration into a tube to maintain a mercury column at 40 mm, thereby reducing blood flow into the thorax.1,2
They concluded that this orthostatic tachycardia syndrome seemed similar to “effort syndrome, irritable heart, or neurocirculatory asthenia” the synonyms of the day for what we now call CFS.
McLean and Allen reported that patients improved by increasing their intake of fluids and sodium, and by sleeping with the head of the bed elevated. The head-up bed may have helped to conserve intravascular volume by reducing blood flow to the kidney at night. It is a medical curiosity that these detailed observations were largely ignored for several decades.
Read the complete article at: