B4-004 Cardiovascular Control Mechanisms Flashcards
3 reasons for changing blood vessel diameter
- to change local blood flow
- to change TPR
- to change CO
changes in local blood flow allow for discrete arterial dilation such as
GI vasodilation during a meal
erection
local arterial dilation [….] resistance, so local flow is […]
decreases; increased
results in no significant change in TPR or MAP
change to local blood flow
TPR is determined by
arterial blood vessel diameters in vascular beds
mainly renal, GI, and skeletal muscle
changing TPR can compensate for
changes in aterial pressure due to standing or blood loss
causes reduced blood to brain
MAP=
CO x TPR
if TPR is increased by arterial vasoconstriction and CO stays the same, MAP will
increase
do increases in TPR normally decrease CO?
no
veins and venules store about […] of total blood volume
2/3
because the heart is a Starling pump, increased venous return increases
cardiac output
venous smooth muscle contractions return
blood to the heart
increased venous return and cardiac output will increase…
MAP
innervate arterial and venous smooth muscle
vasomotor nerves
only relevant constrictor nerves
sympathetic nerves
sympathetic noradrenergic nerves only
constrict
excite vascular smooth muscle by NE acting on a1 receptors
sympathetic nerves
increase MAP by increasing TPR
sympathetic nerves
increase MAP by increasing venous return
sympathetic nerves
induce discrete dilation via NO
parasympathetic nerves
won’t affect TPR under normal conditions
level of activity of nerves and targets
tone
determined by the balance between vasoconstrictor influences and vasodilation influences
vascular tone
determined by concurrent dischange of excitatory sympathetic and inhibitory parasympathetic nerves
cardiac tone
heart rate is increased by […] sympathetic discharge and/or […] parasympathetic discharge
increasing; decreasing
to change blood pressure/output, change
cardiovascular tone
when horizontal, the body is […] hydrostatic column
20cm
in upright position, hydrostatic column is
180 cm
as a result of increased hydrostatic pressure, veins in lower body
standing
distend leading to venous pooling
[…] mL of blood is lost from venous return in the first few minutes after standing
700
decreased venous return leads to
decreased cardiac output,
which leads to decreased MAP
arterial pressure below […] is insufficent to maintain neural activity
90/60 mmHg
result of lost somatic motor control due to diminshed cardiac output
syncope
when cardiac output is diminshed, arterial blood pressure can be maintained by
arterial vasoconstriction
venoconstriction
increased cardiac tone
sympathetic contraction of venous smooth muscle reduces
compliance and capacitance,
forces blood back to heart
arterial vasoconstriction increases TPR, leading to
increased MAP
venoconstriction causes increased CO, leading to
increased MAP
by increasing cardiac sympathetic tone and decreasing vagal parasympathetic tone, heart rate and force of contraction
increase,
making the heart a more effective pump
increased cardiac tone leads to increased
CO
stretch receptors located on vessel walls that tell the brain to modulate autonomic CV tone
baroreceptors
measure venous return
cardiopulmonary baroreceptors
located in right atria, vena cava, and pulmonary vessels
cardiopulmonary baroreceptors
“low pressure” receptors
cardiopulmonary baroreceptors
located in aortic arch and carotid sinus
arterial baroreceptors
assess blood flow to entire body and brain
arterial baroreceptors
“high pressure” receptors
arterial baroreceptors
decreased MAP leads to […] baroreceptor stretch
decreased
decreased baroreceptor stretch leads to
decreased vagal/glossopharyngeal afferent nerve firing
decreased afferent axon firing leads to
decreased firing in nucleus of tractus solitarius
decreased firing in nucleus of tractus solitarius leads to
decreased stimulation of preganglionic cardiac parasympathetic axons in DMV and NA
decreased stimulation of preganglionic cardiac parasympathetic axons in DMV and NA leads to
decreased cholinergic inhibition of the heart
decreased firing in NTS leads to
decreased inhibition of C1
decreased inhibition of C1 leads to
firing of sympathetic nerves to the heart and vasculature
baroreflex activates the SNS without
large effects on adrenomedullary secretion
baroreflex selectively increases resistance in which arteriolar beds?
- renal
- splanchnic
- cutaneous
- skeletal muscle
primary mechanism maintaining MAP under normal conditions
baroreflex
nerves are “buffer nerves”
if cut, more variablity in BP, but no significant change in set point
baroreflex
the baroreflex can be overridden by what?
pain and emotions
- mainly involved in respiration
- active when MAP falls below 60 mmHg
- detects low O2 in carotid and aortic body
chemoreflex
- reduced perfusion of the medulla
- results in discharge of C1
- final line of defense to restore MAP and CO
central ischemic response
when ICP is abnormally high, cerebral vessels collapse, brain perfusion stops and CIR is initiated, this is called?
cushing reaction
inability to compensate for reduced CO associated with upright posture
orthostatic hypotension
orthostatic hypertension can be caused by:
- CNS diseases
- postganglionic axon degeneration
- degeneration of postganglionic sympathetic neurons
- variant of orthostatic hypotension
- characterized by rapid heart rate, dizziness and fatigue
POTS
abnormal sensitivity of the carotid sinus baroreceptors to touch or stretch
carotid sinus syndrome
slight pressure to the neck is perceived as high blood pressure, leading to vagal slowing of heart and fainting
carotid sinus syndrome
abnormally robust response to emotional stimuli leading to withdrawal of vasomotor tone and vagal parasympathetic activation
vasovagal syncope
may be a vestige of an adaptive response for dealing with danger
playing dead
vasovagal syncope
represent short term regulator mechanism
nerves
represent intermediate-term effects
circulating hormones
represent long term regulatory effects
factors effecting volume
- released into circulation
- augments sympathetic nervous system during “fight or flight”
epinephrine
- activates all adrenoreceptors, including b2 receptors
- elicitis skeletal muscle vasodilation
epinephrine
adrenomedullary catechloamine release is not strongly affected by
baroreceptors
exerts intermediate CV control via baroreceptor mediated release
ADH
potent vasocontrictor for both arterioles and veins
ADH
increases plasma volume by reducing urine output
ADH
increased by diminished renal blood flow and sympathetic activation
plasma renin (Ang II)
intermediate effects on CV control via direct action on arteriolar smooth muscle
Ang II
mediates long term volume increases by directly suppressing urine formation and indirectly by causing aldosterone release from adrenal cortex
Ang II
augments NE release from sympathetic varicosities
Ang II
stored in atrial myocardial cells
ANP
elicited by increased plasma volume causing atrial stretching
ANP
acts on kidney to induce sodium excretion into the urine to reduce plasma volume and blood pressure
ANP
if sympathetic neurons are compromised what key function is lost?
vasoconstriction
–> decreased TPR
after taking the drug:
- cardiac output is increased
- total peripheral resistance is unchanged
- central venous pressure is increased
- heart rate is unchanged
what kind of drug?
mineralcorticoid like volume expander
an Alpha 1 adrenoreceptor agonist would increase
TPR
a beta 2 adrenoreceptor agonist would decrease
TPR
what kind of drug?
will decrease
* cardiac output
* TPR
* central venous pressure.
ganglionic blocker
- lost sensation in hands/feet
- does not sweat
- becomes light headed standing rapidly
elevated ADH
sympathetic innervation to the kidney is the major means for
increasing TPR
expansion of plasma volume will result in what hormone changes?
- decreased Ang II
- increased ANP
- decreased epi
- decreased ADH
