Mrs Johnson has suffered blood loss secondary to injury sustained in an automobile accident. She also are manifesting the signs of tachycardia and a fine scarcely perceptible pulse. One would expect that her blood pressure would have fallen. However, her blood pressure has been maintained within the normal adult range ( Systolic;90-120 mm Hg /Diastolic 60-90 mm Hg.). Compensatory mechanisms that have maintained her blood pressure include some of the following: 1. Baroreceptor and chemoreceptor sympathetic reflexes 2. AdrenalCathecholeamine neurotransmitter/hormonal effects 3. Hypothalamic-pituitary hormone effect 4. Kidney hormone Actions Adrenal cortex hormone activity The initial fall in blood volume (and pressure) at the start of the hemorrhaging would be detected by baroreceptors as a change in vascular wall stretch. The reflex sympathetic activity of the baroreceptor arc would cause vasoconstriction especially in the cutaneous and splanchnic arterial and cutaneous. plexuses. This would concentrate blood in the heart and cerebral circulation. Systemic increase in sympathetic tone would result in increased vascular resistance tachycardia and maintenance of adequate cardiac output. Vosoconstriction would induce regional hypoxia and possibly acidosis and these conditions would activate the chemoreceptors. Chemoreceptor response would stimulate responses to boost baroreceptor activity --raise heart rate and increase vasoconstriction. Besides the neural responses to hypovolemia, The medullary centers --cardiovascular and vasomotor centers would also respond; the vasomotor center to increase vasoconstriction and the cardioacceleratory center to increase heart rate and force of cardiac contraction. The body can easily reflexly compensate for acute blood loss of not more 15% of blood volume, if it lasts for a short time. However if the blood loss is prolonged, ad exceeds 20% other mechanisms are employed to lessen the risk of progression to irreversible hypovolemic shock. The Neurotransmitter-hormonal factors; Vasopressin synthesized by the hypothalsmus Adrenal catecholamines Adrenal aldosterone ( mineralocorticoid) Kidney hormones: renin, angiotensin II, aldosterone
Work Step by Step
The baroreceptor and chemoreceptor reflexes respond to changes in blood pressure ( stretch ) and acidity(pH) respectively. They counter threatened blood pressure loss by sympathetic stimultation of the heart and blood vessels that results in tachycardia, increased vascular constriction , increased peripheral resistance, stronger cardiac muscle contractions . All effects hat work to support blood pressure. Vasoconstriction and release of catecholamines foods the vascular system with adrenergic neurotransmitters. By binding to adrenergic receptors in the vascular system these hormones reinforce the sympathetic effects of the neural reflexes--vasoconstriction, cardiac stimulation and increase in blood pressure. If blood loss is high enough the kidneys are stimulated to secrete renin. Renin causes the release of Angiotensin I, and angiotensin converting enzyme (ACE). The latter catalyzes the synthesis of Angiotensin II. Angiotensin II induces the release of the hypothalamic hormone vasopressin(ADH) from the posterior pituitary. The anti-diuretic hormone and the adrenal mineralocorticoid , aldosterone, combine activities to boost blood volume , and cardiac output (CO) . These effects support blood pressure. In a later stage of hemorrhage, decrease in capillary hydrostatic pressure(HPc)-- resulting in a decrease in net filtration pressure(NFP)-- together with a relative increase in capillary oncotic pressure(OPc), will result in transcapillary filling. This means that fluid from the interstitial space will be drawn into the vascular space to increase vascular volume and raise blood pressure.