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95 Cards in this Set

  • Front
  • Back
what is responsible for rapid control of arterial blood pressure (seconds to minutes)
*baroreceptor reflexes

*chemoreceptor reflexes

*CNS ischemic response
what is responsible for intermediate control of arterial blood pressure (minutes to hours)
*renin-aniotensin system

*vascular stress-relaxation

*cap fluid shift
what is responsible for long term control of arterial blood pressure
renal body fluid mechanisms
nervous control of the circulation plays a key role in what
*redistribution of blood flow to various tissues throughout the body

*variations in HR & contractility

*producing rapid changes in systemic BP
the sympathetic NS has what cardiovascular affects
*HR
*contractility
*peripheral vascular resistance
*venous tone
*stimuation of renin release
the PS nervous system has what cardiovascular effects
*HR

*limited effect on contractility
which has more CV effect sympathetic of parasympathetic NS
sympathetic
what is the adrenal medulla
modified sympathetic ganglion
what is the 'hallmark" of the SNS
amplification of response
sympathetic fibers travel down spinal cord to exit ventral root and then can do one of what 3 things
1-synapse w/ post-ganglionic neuron

2-travel up or down the chain & synapse w/ post-ganglonic neurons at other levels

3-pass direclty out to collateral ganglion & synapse there
sympathetic stimulation of venous system causes what to occur
*increased venous return

*increased filling pressures

*increased CO
if you have sympathetic stimulation of arterial side what occurs
redistribution of that blood flow from that tissue to another tissue by decreasing blood flow there (except in skeletal muscle)
where are parasympathetic fibers distributed to the heart
*SA node

*AV node

*lesser extent to the atria
where in the heart is there LITTLE or NO parasympathetic distribution
the ventricles
what is the primary PNS effect in the heart
CHRONOTROPIC with little effect on contractility
where are sympathetic fibers distributed in the heart
*SA and AV node

*atria

*ventricles
how are sympathetic fibers distributed in the heart
via the stellate ganglia
what is the relationship b/t SNS and coronary vessels
good evidence for SNS regulation of small coronary resistance and larger conductance vessels
how are parasympathetic fibers distributed to the heart
via the vagus
what kind of sympathetic tone is occuring in the heart at all times and why
BASELINE tone--so there is firing of some sympathetic neurons at all times

-without baseline tone CO falls
where is the CNS vasomotor center located
in the medulla and caudal 1/3 of pons
how does the CNS vasomotor center transmit parasympathetic impulses to the heart
via CN X (vagus)
how does the CNS vasomotor center transmit sympathetic impulses to the heart and blood vessels
via the spinal cord
what does the vasoconstrictor area of the CNS vasomotor center do
excites preganglionic sympathetic vasoconstrictor fibers

(increase sympathetic outflow)
what does the vasodilator area of the CNS vasomotor center do
inhibits activity of the vasoconstrictor area
what does the sensory area of the CNS vasomotor center do
receives input from CN IX (glossopharyngeal)and X

-sends output to both the vasoconstrictor & vasodilator areas
how is sympathetic vasoconstrictor tone maintained
by continuous slow firing of impulses from the vasoconstrictor area
continuous slow firing from the vasoconstrictor area results in what?

this allows for what?
*results in partial contraction of blood vessels

*allows modulation up or down
what is the hormonal feedback loop for BP control
renin-angiotensin system
what is the mechanism for vasoconstriction
*release of NE from postganglionic nerves

*sympathetic stimulation of adrenal medulla
release of NE from postganglionic nerve endings causes what to occur
activation of alpha adrenergic receptors on vascular smooth muscle

(in everything but skeletal muscle)
sympathetic stimulation of the adrenal medulla will result in what
release of NE and epi into the circulation
in most vascular smooth muscle there is what type of receptor?

activation of this receptor causes what to occur?
*a1 receptor

*vasoCONSTRICTION
in resp, uterine and skeletal smooth muscle there is what type of receptor?

activation of this receptor causes what to occur?
*b2

*vasoDILATION
whether you get vasodilation or vasoconstriction in a tissue is a function of what
the receptor that is predominant
sympathetic stimulation in the lungs will cause what to occur
bronchoDILATION
vasodilation is controlled by what
anterior hypothalamus
vasodilation is thought to be mediated by what
epi released from vasoDILATOR fibers activating skeletal muscle b2 receptors
what type of effect does the vasodilation mech have
(major or minor)
relativey MINOR
what mechanism is thought to contribute to vasovagal syncope
vasodilation mech
the vasodilation mech may allow what type of increase in muscle blood flow prior to local metabolic control
anticipatory
rapid increase in BP (5-10sec) depends on what mechanisms
*arteriolar constriction leading to increased PVR

*venous constriction leading to increased preload & stretch

*SNS stimulation of HR and contractility

*inhibition of PS vagal outflow
BP typically increases how much with heavy exercise
30-40%
what are baroreceptors also called
stretch receptors
where are baroreceptors located
widespread throughout large cervical and thoracic arteries
where are the highest concentrations of baroreceptors(stretch receptors)
at the carotid bifurcation (carotid sinuses) and aortic arch
how do baroreceptors(stretch receptors) operate
by modulating frequency of firing (increase freq of impulses)
carotid sinus baroreceptor impulses travel via what
herings nerve to glossopharyngeal nerve then to vasomotor center
when do carotid sinus baroreceptors begin to fire (work)
~ 50 mmHg
aortic arch baroreceptor impulses travel via what
vagus nerve
aortic arch baroreceptors begin to fire (work) when
~ 30 mmHg
what is the rate of response of baroreceptors
extremely rapid
when do baroreceptors have a greater response
to a rapidly changing BP
when does the greatest change in impulse frequency occur with baroreceptors
within the normal range of BP
activation of stretch receptors results in what
*inhibition of the vasoconstrictor center

*increased vagal outflow
the final result of activation of stretch receptors is what
*arteriolar and venous dilation

*decreased contractility and HR
in EARLY autonomic dysfunction is it PS or sympathetic dysfunction
PARASYMPATHETIC

-evidenced by HR
in LATER autonomic dysfunction is it PS or sympathetic dysfunction
SYMPATHETIC

-evidenced by BP
what in the body is considered the pressure buffer system and why
*the baroreceptors

*they fxn as a pressure buffer maintaining BP within a narrower range
why are barorecptors not as important in LONG term BP control
d/t to "resetting" of baroreceptors to the new pressure
when a baroreceptor "resets" when does this occur
begins within minutes and becomes complete over a period of 1-2 days
how may baroreceptors produce some LONG term blood pressure control
through interaction with the renin-aniotension aldosterone system
where are chemoreceptors located
*carotid bifurcations(carotid bodies)

*aortic arch(aortic bodies)
what do chemoreceptors respond to
*DECREASED o2

*INCREASED co2

*INCREASED H+ ion
how do chemoreceptors transmit impulses
via

*herings nerve-glossopharyngeal

*vagus
what effects do chemoreceptors produce
*excitation of the vasomotor center

*increased resp drive
how to chemoreceptors function in relation to baroreceptors
they are a backup to baroreceptors

-they work at a little bit lower BP
where are low-pressure (atrial) receptors located
*atria

*pulmonary arteries
what do low-pressure (atrial) receptors respond to
changes in VOLUME

(not pressure)
what effects to low-pressue (atrial) receptors produce
responses similar to baroreceptor responses
what is the volume reflex
(aka atrial reflex)

atrial stretch d/t increased blood volume
what does the volume reflex produce
*reflex dilation of renal Afferent arterioles

*signaling to hypothalamus to DECREASE adh secretion

*INCREASED release of atrial natriutetic peptide
what occurs with dilation of Afferent renal arterioles
increased renal filtration and get rid of more fluid
what occurs with decreased ADH secretion
decreased fluid and salt reabsorption
what occurs with increased release of atrial natriuretic peptide
increase in fluid loss
what is the bainbridge reflex
(aka atrial)

increased right sided filling pressure produces 2 effects on HR
1-DIRECT stretch on SA node
2-stretch receptors located in R atrium & cavoatrial junction are stimulated
a direct stretch of SA node results in what
a 15% increase in HR
when stretch receptors in R atrium and cavoatrial junction are stimulated what occurs
*vagal afferent impules travel to medulla w/ subsequent
-decrease in efferent PS activity
-increase in SNS activity

*results in increased HR and contractility
when stretch receptors in R atrium and cavoatrial junction are stimulated how much can HR increase
40-60%
what is the CNS ischemic response
(vasomotor centers are getting ischemic)

dramatic increase in BP in response to a decrease in blood flow to vasomotor center sig enough to impair removal of CO2
the CNS ischemic response produces what effect
*marked stimulation of the vasoconstrictor & cardioaccelerator neurons
the CNS ischemic response may produce what type of sympathetic reponse
a sympathetic discharge severe enough to completely shut down some peripheral vessels (i.e. kidneys)
what is the cushing reflex
CNS ischemic response produced by CSF pressure approaching or exceeding arterial pressure and thereby compromising CNS blood flow
what is the valsalva maneuver
forced expiration against a closed glottis
during a valsalva maneuver what occurs
*increased intrathoracic pressure

*increased CVP

*decreased venous return
as a result of vasalva maneuver what will happen to CO and BP
they will fall
during the valsalva maneuver baroreceptors will do what to HR and contractility
increase them
after the valsalva maneuver what happens to HR and contractility
the opposite--they decrease
what is the oculocardiac reflex produced by
*pressure on the globe

*traction on surrounding structures (muscles)
what is the pathway for the oculocardiac reflex
ciliary nerves-->trigeminal nerve-->gasserian ganglion
what does the oculocardiac reflex result in
increased parasympathetic and PROUNOUNCED bradycardia
what is the incidence of the oculocardiac reflex
30-90% in opthlamic sx
what is the management of the oculocardiac reflex
*the reflex will fatigue with repeated epidodes

*antimuscarinics like atropine or glycopyrrolate
what is the abdominal compression reflex
contraction of abd skeleltal muscle following initition of a baroreceptor or chemoreceptor reflex
what results from the abdominal compression reflex
compression of the venous reserviors increasing venous return & subsequently cardiac output & BP