Background Material
When the autonomic nervous system fails, the homeostatic control of blood pressure is disturbed. The site of the lesions can be at several levels from the hypothalamus to the periphery. The neurological pathways involved in the regulation of blood pressure are indeed complicated and I would refer the reader to specialty texts for the detailed information. Keeping it simple, there are cortical, limbic, anterior and posterior hypothalamic and medullary centers at which input from the carotid sinus and other afferents can be integrated, and the output through the vagus and sympathetic system to the heart and blood vessels may be coordinated.
In autonomic nervous system dysfunction or failure in humans, the baroreceptors, functioning as feedback transducers, do not produce the required responses in the effectors, the resistance and capacity vessels, or the heart and the kidneys. This causes both a change in the "set point" pressure and instability in the response to various stresses. Defects in the cardiovascular reflexes affect short-term adjustment, but long-term compensatory changes of blood volume (which are more difficult to test), but are equally important.
I will review and list in this two-part series the methods available to the student and doctor, which are selected for their simplicity and practical usefulness in a typical chiropractic office. Since autonomic function normally deteriorates with aging, it is a good idea to keep accurate records of conditions and ages to create a set of "aging normals."
Postural Hypotension
When a fall in systolic pressure of more than 20mm on standing is found in a patient with symptoms, further investigation is justified. The instability of blood pressure in autonomic dysfunction or failure is due partly to a lack of baroreflex control, but most likely to super-sensitivity of partially denervated vessels to the transmitter noradrenalin. This may cause recumbent hypotension, leading to hypertensive retinopathy or even cerebral hemorrhage. Investigation of cardiac function has shown that in autonomic dysfunction or failure, cardiac output falls on head uptilt as venous pressure is reduced, due to pooling of blood in the legs. Blood pressure falls during exercise, even though the effect of gravity is eliminated when the patient is recumbent. This is due to a lack of vasoconstriction, which normally occurs in other vascular beds during exercise that compensate for the vasodilatation in exercising muscles.
There are three principle systems of autonomic fibers, which protect against postural hypotension. The most important are the (the first system) sympathetic efferent fibers to "capacity and resistance" vessels in muscles and the splanchnic area, and also the kidneys, affecting renin release. (As a point of differential diagnosis, during your case history-taking, a lumbar sympathectomy has little effect on blood pressure, and even a combined lumbar and cervical sympathectomy has only a transient effect) The splanchnic area is of critical importance and loss of the major part of the total sympathetic outflow is most likely necessary before postural hypotension occurs. Less important, but worth mentioning, are the sympathetic cardioaccelerator fibers and the parasympathetic efferent fibers to the heart.
Postural hypotension occurs with any major lesion of the sympathetic efferent fibers (This would be a very good time to refresh your memory of the normal anatomy of the sympathetic nervous system and, as well, the dorsal horn of the spinal cord.). A diagnostic point is that there is no overshoot after the Valsalva maneuver, as in a normal subject.
Sympathetic Efferent Fibers to the Heart
The second system protecting against postural hypotension, comprised of the sympathetic cardiac efferents fibers, is tested by tilting, cortical arousal and isometric exercise. The tachycardia on tilting and on stress or exercise is probably mediated by similar sympathetic efferent pathways, though different vascular beds are involved.
Parasympathetic Efferent Fibers to the Heart
The third relevant reflex system protecting against orthostaic hypotension is the parasympathetic rate of control of the heart that is, in functional terms, not as important. Parasympathetic function may be tested by the bradycardia on carotid massage. The response is usually absent in autonomic dysfunction/failure.
The Site of the Lesion and the Reflex Arc
The series of tests, to be noted in part two of this series, appear to be for efferent pathways solely, but most involve reflex arcs, and therefore have central and afferent connections as well. If postural hypotension and an abnormal Valsalva maneuver are demonstrated, then it would be a challenging point of differential diagnosis to determine whether or not the lesion is afferent, or efferent, or both. If the vasoconstrictor response to stress is entirely preserved, the efferent limb must be intact and the lesion afferent or central. If the sweating response to generalized body heating is preserved, it can be argued, by analogy, that the lesion is probably afferent since sweat glands are innervated by sympathetic (cholinergic) fibers.
There are, of course, no single lesions in autonomic dysfunction or failure; lesions can occur at more than one site, are progressive, and may be partial rather than complete. Moreover, most tests give information about only one part of an effector mechanism; for example, the preservation of the pressor response in one forearm does not mean that it is spared in the remainder of that limb or in the circulation as a whole. It is not usually possible in the presence of an efferent lesion to diagnose with certainty the presence of another lesion of the afferent side of the arc.
Note: My next article will discuss tests, including: cardiovascular reflexes; sweating; selected tests of autonomic dysfunction; and principles of localization in autonomic failure with hypotension.
For those interested in further readings on this topic, I would recommend Clinical Autonomic Disorders, Second Edition, edited by Philip Low, ISBN 0-316-53281-9, Lippincott-Raven, Publishers.
Keith Innes,DC
Assistant Professor
University of Bridgeport
Hartford, Connecticut
