Physiological changes Flashcards
During compensated shock, how may the body attempt to correct heart rate, blood pressure and venous return.
Decreased blood pressure due to shock triggers sympathetic activation via the baroreceptor reflex .
Results in increased heart rate and vasoconstriction.
Release of ADH and Angiotensin II increases blood volume to correct pressure and venous return
What is the mechanism of ADH release due to baroreceptor activity
Cardiopulmonary (stretch) baroreceptors decrease firing during hypovolaemia, signal sent via nucleus tractus solitarius in medulla to hypothalamus. ADH released by posterior pituitary.
Atrial baroreceptor firing usually inhibits adh release, decreased central venous pressure or hypovolaemia reduces atrial baroreceptor firing
How is renin release to the bloodstream stimulated
Sympathetic nerve activation through beta 1 adrenoceptors
Rental artery hypotension caused by systemic hypotension
Decreased sodium delivery to distal tubules of kidney
How does renin change once it is released in the bloodstream
Renin acts upon substrate angiotensin via proteolytic cleavage to form angiotensin I.
Angiotensin Converting Enzyme found in vascular endothelium converts Angiotensin I go angiotensin II
What actions does Angiotensin II fulfill
Increases vascular resistance and arterial pressure by constricting vessels via AT1 receptor activation
Stimulates ADH release
Stimulates thirst centres
Stimulates sodium reabsorption at renal tubular sites
Acts on adrenal cortex to release aldosterone in reading sodium and fluid retention
Stimulates cardiac hypertrophic and vascular hypertrophy
Stimulates noradrenaline release from sympathies nerve endings
How does renin aid in compensating shock
Renin converted to angiotensin II.
Angiotensin II increased blood volume by increasing sodium and water reabsorption at kidneys via direct action and activating ADH and aldosterone release.
Indirect (stimulates thirst centres in brain)
Increases systemic vascular resistance by constricting resistance vessels by type 1 angiotensin II receptors on blood vessels.
What are the physiological goals during compensated shock
Raise cardiac output
Raise blood pressure
Raise venous return
What is uncompensated shock
State of physiological changes of long term shock, likely leading to irreversible damage
Why may an individual experiencing uncompensated shock suffer circulatory collapse
Build up of waste products and hypoxia in myocardium can irreversibly damage heart leading to progressive heart failure
