Venous Structure/Hemorrhage Flashcards
Systemic veins act as…
blood reservoir
Vein wall structure
Little inherent tone, low R, high distensibility, stretch to accommodate excess volume, little elasticity, valves
When does the venous reservoir need to be tapped?
to increase venous return or cardiac output
Venoconstriction
increases VR
Venous sympathetic constriction
small change in P but no change in R => increased flow back to heart and increased flow downstream
Compliance
ability of vessel to distend & increase volume with little change in transmural pressure
vessel compliance…
true up to a certain volume. with a higher volume, there is only so much distention the vein can do and then it starts acting like an artery.
What does sympathetic discharge do to venous tone?
INCREASES it.
How does sympathetic discharge increase venous tone?
decreases BV => decrease MAP => CNS sympathetic discharge => venoconstriction
Venoconstriction allows
body to tolerate 20% BV loss & maintain normal circulatory function
(restore MAP to normal levels)
Factors that enhance short term venous return
- Cardiac contraction generated driving pressure
- Sympathetically induced venous vasoconstriction
- Skeletal mm. activity
- Venous valves
- Respiratory activity
- Cardiac suction
Sympathetically induced venoconstriction occurs based on
norepinephrine binds to adrenergic receptors => constrictions
Skeletal muscle activity (muscle pump)
contraction compresses veins which decreases venous capacity which increases venous pressure.
Venous valves
- prevent back flow of blood
- spaced at 2-4 cm intervals
- effective against gravitational influences
Respiratory activity (respiratory pump)
- chest activity P~3 to 5 mmHg < Patm
- peripheral vv. at Patm
- change P promotes VR
- breath faster & deeper during excercising -> ^ VR
Cardiac suction (during exercise)
- during vigorous ventricular contraction, AV valve drawn downward
- enlarges atrial cavity => drop in atrial P transiently
- CREATES change in P from venous system into atria
Factors that facilitate venous return in the long term
increase in blood volume
How does an increase in blood volume facilitate venous return?
- passive bulk flow shift of fluid from ISF into plasma
- salt and water retention in kidney
ST BP Regulation control mechanisms
- high pressure baroreceptors
- chemoreceptors
- cardiopulmonary baroreceptors (low pressure)
LT BP Regulation control Mechanisms
- Anti-diuretic hormone (vasopressin)
- Renin-angiotensin-aldosterone
- Natriuretic peptides
What is the primary variable controlled by the CV system?
MAP
basis for Korotkoff sounds
indirect auscultatory measurement of bp.
noise = spurt of blood hitting a static column of blood downstream (systolic P)
Diastolic P = when it stops making noise
Physical determinants of MAP
blood volume and elasticity of large aa.
rate of inflow from heart vs. rate of outflow to periphery
What happens to systolic pressure if the artery is rigid?
it is higher!
What are the physiological determinants of MAP?
CO and SVR
MAP = CO x SVR
SVR’s purpose in determining MAP
when a vascular bed needs more blood it can dilate & get more blood. P upstream is high enough to allow this!
If you ^ SVR,
Flow decreases downstream to organs while elevating upstream P
ST MAP adjustments occur based on
autonomic influences on heart, vessels, and adrenal medulla
changes CO and SVR
LT adjustments to MAP based on
changes to salt & H2O balance to restore BLOOD VOLUME
-alters mechanisms of urine output and thirst
High Pressure Baroreceptors
sense stretch in vascular walls
Location of barareceptors
- Carotid sinus
2. Aortic arch
Why do 2 baroreceptors exist?
for redundancy and for serving the brain & rest of body.
Carotid sinus baroreceptor
sends signals to medulla of brain
Aortic arch baroreceptor
send signal via vagus n. to medulla
Where are baroreceptor impulses sent to?
cardiovascular control center in MEDULLA of brainstem
Frequency of baroreceptor impulses do what?
relay MAP info to CV control center
How does baroreceptor impulse firing increase?
stretch in vessel walls increases which leads to ^AP to ^CO
Which baroreceptors are the most effective in the reflex?
carotid sinus baroreceptors
Why do carotid sinus baroreceptors do a good job maintaining MAP?
the signals go to the brain, which is IMPORTANT
What downstream effectors respond to baroreflex to maintain MAP
heart, arterioles, veins, adrenal medulla, kidney
What happens in heart when baroreflex fires?
it pumps harder and CO increases
What happens in the adrenal medulla when baroreflex fires?
it reduces epinephrine and norepinephrine
What happens in kidney when baroreflex fires?
norepinephrine stimulates B-1 on kidneys => release of renin => Angiotensin II made
What happens in veins when baroreflex fires?
venous return increases
peripheral chemoreceptors are…
proximal to but DISTINCT from arterial baroreceptors
Types of Peripheral Chemoreceptors
aortic bodies
carotid bodies
What do the aortic and carotid bodies do?
sense O2, CO2, pH and send signals to respirating centers.
-can effect MAP though-
When do chemoreceptors play a role in MAP regulation?
ONLY during severe hypoxia
chemoreceptors are…
secondary receptors.
baroreceptors are
primary receptors
Primary role of chemoreceptors
regulate respiration to ^ O2 intake or blow off more CO2
peripheral chemoreceptors are MOST sensitive to…
changes in O2
how do peripheral chemoreceptors work?
example
decrease PO2, ^PCO2 or decrease blood pH => ^SVR
Central chemoreceptor Types
Medulla
central chemoreceptors are most sensitive to…
changes in CO2 & pH
central chemoreceptor mechanisms
example
^PCO2 or decrease pH of CSF => ^ SVR
What do low-pressure (volume) baroreceptors detect?
‘fullness’ of circulation
low-pressure (volume) baroreceptors are…
long term regulators
purpose of low-pressure baroreceptors
- eliminate or retain fluid at kidneys.
- distention depends on VR
What happens if there is a high volume detected by low-pressure baroreceptors?
high V => decrease in renal SNA => ^GFR => decrease renal reabsorption of fluid => decreased renin release => decreased SVR
What happens if there is a low volume detected by low-pressure baroreceptors?
low V => ^ renal SNA => decreased GFR => ^renal absorption of fluid => ^renin release => ^SVR
types of LT humoral control mechanisms for MAP
~Anti-diuretic hormone (vasopressin)
~Renin-angiotensin-aldosterone
~Natriuretic peptides
Function of LT humoral control mechanisms for MAP
to maintain normal MAP via regulation of ECV
GFR =
glomerular filtration rate
Effective circulating blood volume (ECV)
functional blood volume that is effectively perfusing the tissues
(volume of blood in arterial system)
Anti-diuretic hormone secretion determined by…
high- and low-pressure baroreceptors & osmoreceptors
Where are Anti-Diuretic Hormones (ADH) made?
hypothalamus
Where are ADHs stored?
in pituitary
What does ADH cause?
water reabsorption at kidney & vasoconstriction
Renin-angiotensis-aldosterone system does what?
increases SVR, wather, & salt retention at kidney
What happens when perfusion pressure decreases or NaCl increases?
^ renin
What happens when perfusion pressure increases or NaCl decreases?
renin decreases
What do juxtaglomerular cells of kidney do?
synthesize, store, & release renin
ACE =
angiotensin converting enzyme
Natriuretic peptides are secreted in response to
cardiac distention
What would be the predicted physiologic response to cardiac distention/NP secretion?
LT: Stimulate H2O & Na excretion in kidney
ST: 1. Decrease renin, ADH, Ang II, Aldosterone
2. Vasodilation to decrease MAP & @ arteriole => ^ filtration & fluid removal
Hemorrhage is most common cause of
hypovolemic circulatory shock
hypovolemic circulatory shock
inability to get enough blood to tissue
how does hemorrhage cause hypovolemic circulatory shock?
loss of blood volume -> decreased cardiac filling pressure -> decrease in venous return -> decreased cardiac output
Hemorrhage and MAP/CO
MAP/CO rapidly fall with respect to the amount of hemorrhage that occurs. They are inversely related at larger amounts of hemorrhage. (more hemorrhage, less CO/MAP)
When the body loses a smaller amount of blood, a
sympathetic discharge keeps MAP @ fairly normal levels.
When the body loses more blood, it
cannot compensate for the loss as well as when its lost a little bit of blood. MAP can be higher and even plateau, but eventually it will die completely.
What is the plateau phase of CO/MAP that occurs during massive hemorrhage?
the body’s last effort to save itself via a massive sympathetic discharge. (chemoreceptor response)
How does autoregulation play into hemorrhage?
it maintains flow to the brain and heart despite a 1/4 to 1/3 decrease in flow to other organs.
this doesn’t last forever
Critical level
the MAP from below which the body cannot recover from during a hemorrhage without medical intervention.
Levels of hemorrhagic shock
- Nonprogressive
- Progressive
- Irreversible
Nonprogressive hemorrhagic shock
normal circulatory compensatory mechanisms eventually cause full recovery w/o outside therapy
Progressive hemorrhagic shock
without therapy, shock becomes steadily worse until death
Irreversible hemorrhagic shock
shock has progressed to such an extend that all forms of therapy are inadequate to save the patient.
AKA even without medical intervention you cant save animal
What are the factors that compensate for nonprogressive hemorrhagic shock enough to prevent further deterioration of circulation?
baroreflex, central chemoreceptors when MAP < 50 (more powerful thanbaroreflex), ^ renin secretion, angiotensin II, ^ vasopressin secretion, ^ epin. & norep., restore BV
How is BV restored during nonprogressive hemorrhagic shock?
conservation of salt & H2O at kidney, increased thirst, fluid flux from ISF to capillary
Transcapillary refill
fluid from ISF entering capillary beds to aid in restoration of BV during hemorrhage
hemodilution
- evidence of fluid from ISF moving to vasculature.
- cap. oncotic pressure decreases during bleed => dilution of plasma proteins in vascular space b/c H2O is pulled into vasculature & decreases [protein] in vasculature wrt ISF [protein]
What causes progressive hemorrhagic shock?
vicious cycle of CV deterioration.
Cardiac depression
-decrease in coronary blood flow (CBF) below that required to meet metabolic demands of heart
-weakens heart muscle => further decrease in CO (despite ^BP in RA)
=> Progressive deterioration of heart over time
Methods of CV deterioration
- Cardiac depression
- Failure of constrictor response
- Failure of transcapillary refill
- CNS depression
Failure of constrictor response
Occurs with prolonged hypertension:
- Desensitization of a1-receptors (don’t respond well to norep. stimulus)
- Norep. depletion in nerve terminals
- Metabolic vasodilator build-up
What is the effect of metabolic vasodilator build-up?
- stimulates more vasodilation
- lose vasoconstrictor response
Failure of Transcapillary Refill
-Precapillary sphincters fail b/c can’t stay constricted forever
-Arterioles lose resistance
-Venules retain tone for longer b/c of decrease R in aa. & ^R in vv.
=> ^capillary hydrostatic P
An increase in capillary hydrostatic P leads to…
loss of fluid b/c hydrostatic P > colloid osmotic pressure
CNS Depression
Occurs with cerebral ischemia:
-Decreased neural activity in brain
-Weakens sympathetic output
=> Decreased vascular and cardiac responses
What is the MAIN issue with irreversible hemorrhagic shock?
even a transfusion is INCAPABLE of saving patient’s life
What can therapy not overcome in irreversible hemorrhagic shock?
- extensive tissue damage
- destructive enzyme release
- extensive acidosis
What leads to irreversible hemorrhagic shock?
too much blood is lost and the animal has already gone through nonprogressive and progressive hemorrhagic shock WITHOUT any treatment
