C sympathetic stimulation elevation of BP and tachycardia perfusion of the tissues is restored.

C sympathetic stimulation elevation of BP and tachycardia perfusion of the tissues is restored. (ii) Sympathetic stimulation also causes carotid chemo receptor stimulation by causing vasoconstriction of the artery feeding the carotid chemoreceptors. Further, hemorrhagic shock produces hypoxia which also causes chemoraceptor stimulation (particularly if the subject is restless). Chemoreceptor stimulation in turn, produces VMC stimulation. Fall of BP, if of sufficient degree, results in ischemia of the VMC and in turn produces stimulation of VMC (CNS ischemic response, chap. 8 sec. V, see also fig 5.8.1). Stimulation of VMC causes stimulation of sympathetic system elevation of BP restoration of perfusion. Also sympathetic stimulation causes redistribution of blood flow, the cutaneous, splanchnic and muscle blood flow are greatly cut down and the blood thus made available are flown to the brain and heart. Recall sympathetic stimulation, (i) has no effect on brain blood vessels, and (ii) causes coronary dilatation. The sympathetic stimulation produces some well known signs of shock, like pallor and sweating (pallor, because of the cutaneous vaso constriction. sweat glands are supplied by the sympathetic fibers, therefore sympathetic stimulation may lead to sweating and cold clammy skin). Endogenous substances like adrenalin are also liberated (as hemorrhage produces 'stress' and stress causes adrenalin secretion). Adrenalin reinforces the sympathetic activity. II. Tissue fluid shift As the BP falls the capillary blood pressure also falls. However, there is no fall of the colloidal osmotic tension. This causes stoppage of flow of fluid from the capillary to the tissue, or if the fall of BP is greater, the return of the tissue fluid to the capillary is enhanced (see Starling's hypothesis, fig. 1.1.9). This corrects the hypovolemia within the vascular compartment increase in cardiac inflow, and the real follows. III. Conservation of body water Fall of BP leads to lowering of perfusion pressure of the kidney production of renin production of angiotensin production of aldosterone [for details, see chapter on aldosterone, chap. 4 (control of sacretion) sec VI] sodium retention body water retention. It is now known, in stress, the hormone ADH is also secreted in greater amount. This reduces the volume of the urinary output body water conserved hypovolemia corrected. [Cardiovascular shock is a farm of stress. Recall, any deviation from homeostasis is a stress (chap 3 sec I). In massive hemorrhage, massive amounts of ADH is secreted. ADM in high concentration acts as vasopressin which is a powerful visoconstrictior. In addition, local autoregulatory mechanisms are also important. Even if the BP is falling for considerable period. the blood flow of the brain or heart does not fall, although blood flow in the other organs are falling. This is called autoregulation, whose mechanisms have been discussed earlier (chap. 6 sec V, see also fig. 5.10.2). However, if the fall of BP is severe, agtoregulation cannot manage. Compensatory mechanisms are often called 'negative feed back mechanisms', negative, because the results (effects) are in the opposite direction of the causes(chap. 3 sec I). For example, withdrawal of baroreceptor stimulation is caused by the fall of BP but effect of the withdrawal of baroreceptor stimulation is rise of BP A -ve feed back mechanism restores homeostasis, whereas a +ve feed back destabilizes the homeostasis irreversible shock if the shock continues and is not treated promptly, the stags of 'irreversible shock, develops, when the patient dies despite the (late) institution of the correct treatment. It will be seen afterwards, the term irreversible is rather misleading, a better term will be advanced stage of shock'. Causes of the irreversibility. At this stage some +ve feed back mechanisms appear in the scene with the result that there develops a vicious cycle [a cycle of 'vices' or sins; example, an individual begins, say, gambling loses money his financial situation deteriorates with a hope to improve his monetary position, he does more gambling further loss of money). These are: (a) Cardiac damage (i) Even normally, the subendocardial region of myocardium is susceptible to anoxia. When the BP is falling, this danger increases and ultimately subendocardial damages occur further fill of cardiac output (due to subendocardial damage) the vicious cycle operates (ii) A factor called, myocardial depressing factor, is suspected to appear in the circulation during advanced stages of shock. This reduces cardiac contractility vicious cycle, (iii) In advanced stages of shock, the acidosis (see below) develops and depresses the myocardial contractility still further further fall of BP vicious cycle. (b) Acidosis Tissue anoxia leads to accumulation of lactic acid acidosis. The fall of pH causes relaxation of the arteriolar and precapillary sphincter muscles vasodilatation operation of vicious cycle. (c)vToxemia Prolonged spasm or the splanchnic vessels (which develops as a result of compensatory mechanism) intestinal mucosal damage due to lack of 02 massive entry of the intestinal bacteria (through the damaged mucosa) which liberate toxin relaxation of the vascular smooth muscles due to the effect of the bacterial toxin. (Recall, during sympathetic simulation, powerful splanchnic vasospasm develops). (d) VMC ischemia Slight ischemia stimulates the VMC, but massive ischemia kills it. When VMC death sets in, there is sympathetic paralysis precipitate fall of BP. (e) Elderly people generally have artherosclerotic lesions in their coronary"