SHOCK COMPENSATORY CASCADE

6. COMPENSATORY MECHANISM
6.1 The baroreceptors in the aortic arch and carotid sinus receive the signal of falling BP and send less afferent stimuli to the vasomotor centre in the medulla.
This results in enhanced sympathetic tone ending in arteriorlar and venous constriction.
There is increase in the after load and increase in venous
return to the heart (increase pre-load).
The vascular constriction is least in cardiac and cerebral circulation.
The enhanced adrenal medullary output of catacholamines results in
increased heart rate and mycardial contractility.
All these mechanisms improve cardiac output.

6.2 Antidiuretic hormone (ADH) is also released from the
posterior pituitary in response to the hypovolemia.
This ADH produces vaso-constriction in the visceral circulation and
increased re-absorbtion of water from the distal tubules of the
kidney.

6.3 Renin secretion is also stimulated by the hypo-perfusion of
juxta-glomerular apparatus in the kidney.
This leads to formation of angiotensin-I in the liver and later to angiotensin-II in the lungs.
This angiotensin-II is a powerful vasoconstrictor. This
is also a signal for release of aldersterone from the adrenal
cortex.

6.4 The aldersterone is a valuable restorer of circulating volume
by re-absorbtion of sodium from the renal tubules.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review