POSTURAL EFFECTS ON HEART-RATE AND BLOOD-PRESSURE
Article first published online: 10 AUG 1933
© 1933 The Physiological Society
Quarterly Journal of Experimental Physiology
Volume 23, Issue 1, pages 1–33, August 10, 1933
How to Cite
1933), POSTURAL EFFECTS ON HEART-RATE AND BLOOD-PRESSURE. Experimental Physiology, 23 doi: 10.1113/expphysiol.1933.sp000588., (
- Issue published online: 10 AUG 1933
- Article first published online: 10 AUG 1933
- Cited By
The slowed pulse-rate in the horizontal posture as compared with sitting, and the quicker rate in standing as compared with sitting, depend on wholly different mechanisms and may vary independently.
The relative amount of muscular contraction present in these postures has no appreciable effect.
The sitting-lying difference is due to hydrostatic influence acting mainly, if not wholly, through the carotid sinus reflex. Pronounced variation in the activity of this reflex may occur at different periods of the day and on different days; such variations are associated with the absence or marked occurrence of a sitting-lying difference. When the reflex is not active, a change from lying to sitting, or vice versa, causes no change in pulse-rate; the different incidence of gravity on the splanchnic area and changes in the tension of the abdominal wall and in the tone of the back-muscles, etc., are evidently unimportant as regards the pulse-rate, which is not affected by splanchnic adjustment, compensatory as regards blood-pressure, when the trunk is moved into the vertical position.
The sitting-standing difference is associated with hydrostatic influence acting on the altered position of the thighs, horizontal or vertical, in the two postures. The relative position of the leg is unimportant. In the horizontal position, prone, lateral, or supine, variation in the position of the thighs is ineffective; when the upper end of the trunk is elevated to the vertical or to a certain extent from the horizontal, certain changes in the position of the thighs affect the pulse-rate.
The increased heart-rate in the standing position is not accounted for by gravity acting on the capacious splanchnic area, determining a lowering of aortic pressure, for a lowering does not occur in normal subjects; nor is the acceleration dependent on increased tone of the abdominal wall, trunk-muscles, etc., nor upon the position and tension of the muscle-groups of the lower limbs.
The standing-lying difference equals the combined standing-sitting and sitting-lying differences. While the latter is nil, when the carotid sinus reflex is not active, the standing-lying and the standing-sitting differences are equal. These often vary in parallel fashion. The pulse-slowing in certain postures, e.g. in the foot-up position in standing, is associated with the inclination of the thigh.
The squatting posture may cause slowing or acceleration, sometimes showing a definite relation to the carotid sinus reflex. Compression of tissues and vessels is involved in this position.
Artificially induced vascular turgescence of the lower limbs in the sitting or standing, but not in the horizontal, position is attended by increase in pulse-rate.
Artificial occlusion of the circulation in a lower limb leads to a suspension of certain postural effects on the pulse-rate.
Some effects of bending the trunk in certain ways are described.
While standing motionless the pulse-rate is decidedly faster—5 to 10 beats—than when slight, continued movements are kept up in the lower limbs. The action is directly on the circulation in the limbs and reflexly on the heart-rate, not through change in aortic pressure.
Apart from the conditions present in the splanchnic area, the posture and vascular condition of the lower limbs has a marked influence on the pulse-rate. As the effects are evidently not mediated through changes in general (aortic) blood-pressure, they may be assumed to depend on afferent impulses especially related to the position of the thighs, and probably originating from some part of the vascular apparatus under the influence of the hydrostatic factor.
Changes of the thighs from the horizontal to the vertical kneesdown position are much more regularly effective in most subjects than changes from the horizontal to the vertical knees-up. In some subjects, where the latter is effective, opposite effects have been found in the vertical position knees-down (acceleration) and the vertical knees-up (slowing), while intermediate inclinations tend to give intermediate rates. The effects are obviously dependent on the relation of the thighs to the vertical, not directly on their relation to the trunk.
Slight repeated movements and vascular turgescence of the lower limbs are presumed to influence the pulse-rate through afferent impulses.
Not only pulse-rate, but also blood-pressure adjustments in the standing position, are influenced by afferent impulses from the lower limbs.
Static contraction of muscles on a large scale, e.g. with the knees bent as described, soon causes a remarkably large rise of systolic and diastolic blood-pressures, comparable to what may be induced by strenuous muscular exercise, but differing in certain respects in the mechanism of its production.
Marked variation in postural effects on the pulse-rate may occur at different times apart from obvious disturbing causes, and apart from the increased lability ordinarily present in some apparently healthy persons.
It remains to be seen whether a study of postural effects can give information as to developing defects of co-ordination and control in the vascular system, leading up to conditions of persistent high or low pressures, and whether when abnormal levels have been established any differentiation of types is practicable.
Part of the expenses of this inquiry has been defrayed by a grant from the Medical Research Council.