short term control of blood pressure Flashcards
Mechanisms For Controlling Blood Pressure: Aldosterone
hormonal. activation time:hours activation strength: medium
Mechanisms For Controlling Blood Pressure: Baroreceptors
nervous activation time: seconds activation strength: large 7)
Mechanisms For Controlling Blood Pressure: Capillary fluid shift
physiological minutes medium
Mechanisms For Controlling Blood Pressure: Chemoreceptors
nervous seconds medium
Mechanisms For Controlling Blood Pressure: CNS ischemic response
nervous seconds large 11
Mechanisms For Controlling Blood Pressure: renal blood volume pressure control
kidneys hours infinite
Mechanisms For Controlling Blood Pressure: renin angiotensin-vasoconstriction
hormonal minutes medium
Mechanisms For Controlling Blood Pressure:stress relaxation of vasculature
physiologic second medium
cns ischemic response range
0-75
chemreceptors response range
25-115
barreceptors response range
50-225 decrease prssures
renin angiotensin vasocontriction range
30-120
renal blood volume and capillary fluid shift range
work over all pressures.
Parasympathetic
Regulation of heart rate
Small affect on contractility
Minimal regulation of
circulation
sympathetic
Regulation of circulation
Regulation of contractility
vasomotor center
Parasympathetic impulses via vagus nerve (heart) Sympathetic impulses via spinal cord & peripheral sympathetic nerves to all arteries, arterioles, veins
Sympathetic Innervation of Blood Vessels
Arteries, arterioles, venules, veins of most tissues receive
sympathetic innervation
Some metarterioles & precapillary sphincters of mesenteric blood
vessels innervated
Most sympathetic nerve fibers are
vasoconstrictor (few
vasodilator)
Vasoconstriction potent in kidneys, intestines, spleen, and skin
Vasoconstriction weaker in skeletal muscle and brai
When sympathetic impulses sent to blood vessels
impulses
also go to adrenal medulla resulting in secretion of epinephrine
& norepinephrine
Small arteries / arterioles are able
o change resistance / change flow through each tissue
Veins are Able to change
volume held in vessels thus changing venous return
Vasomotor Center - Location
bilateral.
Reticular substance
Medulla
Lower third of pons
Sympathetic impulses via spinal cord and periphereal
go to arteries arterioles and veins.Regulates amount of vascular
constriction AND cardiac
activity (i.e. heart rate &
contractility)
Vasoconstrictor area
Bilateral -Anterolateral part of upper medulla
Sends fibers to all areas of spinal cord
Fibers excite vasoconstrictor neurons of
sympathetic system
Vasodilator area
Bilateral -Anterolateral part of lower medulla
Sends fibers to vasoconstrictor area
Fibers inhibit activity of vasoconstrictor area
Sensory area
Bilateral in tractus solitarus in posterolateral
part of medulla & lower pons
Receives sensory signals from circulatory
system via vagus & glossopharynegeal nerves
Sends output to vasoconstrictor and
vasodilator areas
Allows control of vasoconstrictor / vasodilator areas
based on input from circulatory system
Lateral portions of vasomotor center
Sends excitatory impulses via sympathetic nerves to heart
[increase heart rate & contractility]
Medial portion of vasomotor cente
Sends impulses to dorsal motor nuclei of vagus nerves which
sends parasympathetic impulses to heart [decrease heart
rate & some decrease in contractility]
Vasomotor Center – Cardiac Control normally
increased cardiac activity is stimulated when
vasoconstriction center is stimulated
decreased cardiac activity is stimulated when
vasoconstriction center is inhibited
Sympathetic Vasoconstrictor Tone
Amount of vascular constriction is proportional to
number of impulses sent out by vasoconstrictor area
Increase number of impulses per second – Increased
constriction
Decrease number of impulses per second – Decreased
constriction
Sympathetic Vasoconstrictor Tone under normal conditions
Vasoconstrictor center sending 1.5 to 2.0 impulses per
second
Results in partial constriction – normal vasomotor tone
spinal anesthesia can block
blocks transmission of
sympathetic impulses
from spine to periphery
Vasomotor Center – Control by CNS
Reticular substance of pons, mesencephalon,
diencephalon controls
Lateral / superior portions excite vasomotor center
Medial / inferior portions inhibit vasomotor center
Vasomotor Center – Control by CNS hypothalamus
Posterolateral portions excite vasomotor center
Anterior portion produced mild excitation or inhibition
Depends on which part of anterior portion is stimulated
Vasomotor Center – Control by CNS cerebral cortex
Motor cortex excites vasomotor center
Multiple areas can excite or inhibit depending on specific
area stimulated
General Effect of Nervous Control Able to produce rapid increase in ___ which stimulates and inhibits______
vasoconstrictor area (sympathetic) increases cardiac activity (sympathetic) and inhibits parasympathetic vagal signals to heart
General Effect of Nervous Control physiologic response
Constriction of most arterioles of systemic circulation
Increased SVR Increased MAP
Strong constriction of veins / some constriction of larger
arteries
Transfer volume from veins to arteries Increased venous return
Increased preload Increased stroke volume Increased MAP
Increased cardiac performance
Increased HR (major effect) Increased CO Increased MAP
Increased contractility Increased stroke volume Increased MAP
Baroreceptors are located
in walls of most large arteries of the thorax and neck regions. Many located in wall of the internal carotid arteries above the bifurcation (carotid bodies in carotid sinus) and in wall of aortic arch
Carotid baroreceptors send
impulses
via Hering’s nerves to glossopharyngeal nerves which carry impulses to sensory area of vasomotor center Aortic baroreceptors send impulses to vasomotor center via vagus nerves
Baroreceptors Response to Pressure
Carotid receptors not stimulated until pressure 50 to 60 mmHg Aortic receptors not stimulated until pressure 80 to 90 mmHg Receptors produce greater response when pressure changing (could be twice the response) Stimulates changes in vascular resistance and cardiac performance
Baroreceptors and Long Term Control
Some controversy in terms of their importance
If pressure changes and remains at new level,
baroreceptors will RESET to new level
Takes 1 to 2 days
Will produce normal rate of impulse generate at the
“new” pressure
Happens no matter which way the pressure changes
Long term, may mediate changes in sympathetic
tone to the kidneys
Increased pressure mediate decreased sympathetic
tone to kidneys promotes increases sodium and
water excretion
chemoreceptors sensitive to and located in
lack of oxygen and excess carbon dioxide and
hydrogen ions
Location
Carotid bodies (2) in bifurcation of each common carotid artery
Aortic bodies (1 to 3) adjacent to aorta
chemoreceptors excite
nerve fibers that pass through Hering’s nerves and vagus
nerves to vasomotor center
CHEMORECEPTORS :Nutrient artery to each body
ensures good supply of blood to
sample
Decreased flow through artery causes decrease in oxygen and an
increase in carbon dioxide and hydrogen ions.
Impulse generation increases with decreased flow through
nutrient artery which results in excitation of vasomotor center
Increased impulses from chemoreceptors EXCITE the
vasomotor center
Kick in when pressure falls below 80 mmHg
CNS ISCHEMIC REPSONSE
DIRECT RESPONSE OF VASOMOTOR CENTER DUE TO ISCHEMIA. VERY POWERFUL!!!!! INCREASE BP TO 250. CUTS OFF FLOW TO LESS IMPORTANT TISSUE LIKE KIDNEYS. INITIATED AT 60 RREACHES GREATEST STIMULATION AT 15-20
Atrial / Pulmonary Stretch Receptors
Located
in walls of atria and pulmonary arteries
Low-pressure receptors – similar to baroreceptors of
large systemic arteries
Atrial / Pulmonary Stretch Receptors MINIMIZE
changes in arterial pressure due to sudden
changes in blood volume
Atrial Reflexes and the Kidney (A) PATHWAY
Increased atrial stretch Reflex dilation afferent
arterioles of kidney
Reflex dilation afferent arterioles Increased glomerular
capillary pressure
Increased glomerular capillary pressure Increased
glomerular filtration
Increased glomerular filtration Increased urine output
Increased urine output Decreased circulating blood
volume
Decreased circulating blood volume Decreased venous
return and decreased cardiac output
Atrial Reflexes and the Kidney (B PATHWAY
Increased atrial stretch Signals hypothalamus to
produce less antidiuretic hormone (ADH)
Decreased concentration of ADH Decreased
reabsorption of water from renal tubules
Decreased reabsorption of water Increased urine
output
Increased urine output Decreased circulating blood
volume
Decreased circulating blood volume Decreased
venous return and decreased cardiac output
Bainbridge Reflex
Increase in atrial pressure causes an increase in heart
rate
Part of the response due to direct stretch of the sinus
node (can increase heart rate up to 15%)
An additional 40 to 60% increase caused by
Bainbridge reflex
BAINBRIDGE REFLEX
Increased atrial stretch Increased impulses via vagus
nerves to medulla
Increased impulses to medulla Increased sympathetic
impulses to heart increasing heart rate and contractility
Respiratory Waves
Change in arterial pressure
of 4 to 6 mmHg during each
inspiration/expiration cycle
Change in arterial pressure INSPIRATION
Pressure in thoracic cavity becomes more negative
Blood vessels in chest expand
Expansion of blood vessels decreases venous return which decreases
cardiac output and arterial pressure
CHANGE IN ARTERIAL PRESSURE EXPIRATION
Pressure in thoracic cavity becomes positive
Blood vessels in chest constrict
Constriction of blood vessels increases venous return which increases
cardiac output and arterial pressure
Signals from respiratory center spill over
into vasomotor center
Pressure changes in thoracic vessels due to inspiration/expiration can
stimulate the vascular and atrial stretch receptors
Vasomotor Waves
Possible to see slow oscillation in arterial pressure
waveform of 10 to 40 mmHg
Cycle duration is approximately 7 to 10 seconds
Oscillation Baroreceptor / Chemoreceptor reflexes:
Increased pressure produces increased baroreceptor
response which produces vasodilation (etc.) which
causes the pressure to fall. The decreased pressure
causes a decrease in baroreceptor response which
produced vasoconstriction (etc.) which causes the
pressure to rise. Creates a cycle of pressure oscillations
