Acute hypovolemia in conscious mammals induces a two-phase response: initial sympathetic maintenance of arterial pressure, followed abruptly by sympathetic withdrawal and profound hypotension.
What are the hemodynamic and neurohumoral responses to progressive acute hypovolemia in conscious mammals?
Acute hypovolemia triggers a biphasic physiological response characterized by initial sympathetic compensation followed by abrupt sympathetic withdrawal and hypotension at ~30% volume loss.
In conscious mammals including humans, the neurohumoral and hemodynamic responses to progressive acute hypovolemia have two distinct phases. There is an initial arterial baroreceptor-mediated phase in which the fall in cardiac output is nearly matched by a sympathetically mediated increase in peripheral resistance so that arterial pressure is maintained near normal levels. In most species, adrenal catecholamines and vasopressin contribute little to this phase. Increased renin release appears to augment the sympathetically mediated vasoconstriction. When blood volume has fallen by a critical amount (approximately 30%), a second phase develops abruptly. This phase is characterized by withdrawal of sympathetic vasoconstrictor drive, relative or absolute bradycardia, an increase in release of adrenal catecholamines and vasopressin, and a profound fall in arterial pressure. In rabbits and rats the signal that initiates this phase appears to travel in cardiopulmonary afferents. In dogs and humans its origin is unknown. Central opioidergic and serotonergic mechanisms may be involved.
Schadt et al. (Fri,) conducted a review in Acute hypovolemia. Acute hypovolemia was evaluated on Neurohumoral and hemodynamic responses. Acute hypovolemia in conscious mammals induces a two-phase response: initial sympathetic maintenance of arterial pressure, followed abruptly by sympathetic withdrawal and profound hypotension.