Heart and endocrine changes during central hypovolemia in man.
Animal experiments have shown that severe haemorrhage often is characterized by an initial general increase in sympathetic activity leading to an increase in heart rate and a subsequent vagally mediated, reversible decrease in heart rate. It is likely that the decrease in heart rate is triggered by mechanoreceptors situated in the left ventricle. The receptors are supposed to be activated by a reduction in end-systolic volume occurring as a result of a decrease in venous return concomitant with the initial increase in heart rate. SA vago-vagal reflex elicited from and returning to the heart is thereby activated, resulting in a slowing of the heart. It has been hypothesized that the left ventricular receptors are activated when the ventricle contracts around an almost bloodless chamber. The decrease in heart rate may allow for an increased filling of the heart and an improved coronary perfusion. However, these experimental observations are in clear contradiction to the general description of the regulatory mechanisms operating during haemorrhagic shock in man as presented by authoritative medical, surgical and anesthesiological textbooks. Until now the (over-simplified) notion has been, that progressive haemorrhage results in an increased activation of the sympathetic nervous system leading to an increase in heart rate and that the occurrence of bradycardia was a sign of irreversible shock. The present systematic measurements in patients in haemorrhagic shock showed that the heart rate during severe haemorrhage often was normal (mean value 73 beats/min, range 46-98 beats/min). Simultaneous measurements of plasma concentrations of pancreatic polypeptide (an index of vagal activity) indicated that organs other than the heart also were exposed to increased vagal activity. A marked increase in the plasma concentration of vasopressin was not a constant finding as it was during the experimental-induced hypotensive central hypovolemia. This difference may be due to a decline in the release of vasopressin during prolonged haemorrhage. In order to elucidate essential regulatory mechanisms behind the clinical observations, central hypovolemia was induced experimentally by "head-up tilt", "lower-body negative pressure", "venous tourniquets of the thighs plus haemorrhage", and by epidural anesthesia. The initial stage of central hypovolemia was characterized by an increase in sympathetic nervous activity resulting in an increase in heart rate. Activation of the renin-angiotensin-aldosterone system occurred prior to marked increases in plasma concentrations of vasopressin. During progression of the central hypovolemia a qualitative shift in the regulatory mechanisms was evident.(ABSTRACT TRUNCATED AT 400 WORDS)
Sander Jensen
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K
Institute of Medical Physiology C, University of Copenhagen.
D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure; D001810:Blood Volume; D004702:Endocrine Glands / Q000473:pathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009206:Myocardium / Q000473:pathology*; D011311:Pressoreceptors / Q000502:physiology; D012083:Renin / Q000378:metabolism; D012769:Shock / Q000188:drug therapy / Q000503:physiopathology*; D012771:Shock, Hemorrhagic / Q000503:physiopathology; D014667:Vasopressins / Q000378:metabolism; D001615:beta-Endorphin / Q000378:metabolism
D014667:Vasopressins; D000804:Angiotensin II; D000450:Aldosterone; D001615:beta-Endorphin; D001285:Atropine; D012083:Renin