cardiovascular : blood vessels Flashcards
what is the correlational relationship b/w blood flow and pressure gradient
blood flow= change in pressure (gradient) / Resistance
what does the blood flow depend on
PRESSURE GRADIENT!!!!!
-does not matter what the overall pressure is just the diference between the pressure at the end/beginning
what is resistance
how does it connect to the flow?
measure of hindrance to blood flow through a vessel
Increased resistance means harder to pas blood and a slower flow
what factors impact resistance ??
- blood viscosity (more erythrocytes= more friction between molecules- more resistance)
- vessel length (longer= more resistance)
- vessel diameter (smaller = more resistance)
what lines vessel walls ?
endothelium / endothelial cells. surrounded by smooth muscle and connective tissue
what are the two types of arterial connective tissue fibers and their purspoe
collagen- tensile strength
-elastin- elasticity
how much blood enters arterioles from ventricular systole?
1/3 of the volume! the other 2/3 stay in arteries
what happens right at the end of ventricular systole -> diastole to the arteries
-blood flows in -> pressure increases in arteries->arteries expand -> (aortic valve closes for diastole and allows ) elastic recoil -> increase pressure -> blood enters arterioles
what is blood pressure
force exerted by blood on the vessel wall!!
- depends on volume of blood contained within the vessel and compliance or distensibility of the vessel wallls
- fluctuates in relation to ventricular systole and diastole
how does sphygmomanometer measure bp and what sounds does it make
- indirect measurement - inflatable cuff and a pressure gauge
- pressure is transferred from cuff to BRACHIAL ARTERY
- stethescope placed over brachial artery on inside of elbow- Korotkoff sounds are created by pressure of cuff on brachial artery (like turbulent flow)
- first reading at absence of sound is diastole
- no sound is systolic
what is the main driving force fo rblood flow through the cardiovascular system
mean arterial pressure
diastolic pressure + 1/3 pulse pressure
what establishes the pressure gradient
pressure in arterioles (vs arteries)
what is in the arteriole wlal
little elastic ct, thick layer of smooth muscle
contraction= decrease in radius = increase in resistance = decrease in flow
(precision in control)
what is the blood flow rate vs blood flow velocity
blood flow rate : blood volume passing a particular vessel in a period of time
blood flow velocity: blood volume passing total cross section area of all vessels at that given level of the circulatory system
how do blood flow rate and velocity vary in capillaries
velocity DROPS , but flow rate REMAINS THE SAME!!
how does cardiac output compare to volume of blood in any level of the cardiac system
must be equal
what does the maximum amount of blood received depend on
number and caliber of arterioles supplying that aarea
what are the 2 types of control over arteriolar vasoconstriction and dilation
intrinsic (local)- distribution of cardiac output to specific tissues - using left arm, etc
extrinsic (global) – pressure regulation
what 5 factors produce relaxation of arteriolar smooth muscle under INTRINSIC control?
- decrease in O2
- adenosine release
- increase in co2
- increase in acidity
- k+ (release from contracting skeletal muscles- causes hyperpolarization and relaxation in vessels muscles)
what of the two types of control do endothelial cells provifde? what are their vasoactive factors? and what does each do (3 of them )
INTRINSIC CONTROL - line BV’s and chambers of the heart
- Nitric oxide - potent vasodilator
- endothelin - potent vasoconstrictor
- vascular endothelial growth factor (VEGF) - stimulates new vessel growth (angiogenesis)
what is active hyperemia
intrinsic control type
increasd blood flow in response to enhanced tissue activity (local factors of an organ act on the supplying arteriole)
-increased local metabolic activity
what is reactive hyperemia
intrinsic control type
-increase blood flow post-occlusion (blocking of vessel)
-local blockage of blood supply
what is sympathetic extrinsic control
EXTRINSIC CONTROL!!!!!!
- increased sympathetic activity results in generalized arteriolar vasoconstriction
- vasoconstriction and higher BP in response to sympathetic stimulation is immediately followed with vasodilation of vessels supplying tissues that need more blood!! OVERRIDE
- Tissues with lower blood demands during sympathetic response will not override the sympathetic constrictor effect and will receive less bloood
(the decreased blood flow to all tissues and increase in pressure causes a driving force for blood to flow to all tissues)
where does blood supply decrease during exercise
digestive system, liver, kidneys, and bone
-cardiac output increases but to these it DECREASES
how does blood flow to brain change with cardiac output changes
DOES NOT CHANGE
what mediates sympathetic effects on vessels
extrinsic
sympathetic vasoconstriction is mediated by norepinephrine activity on alpha 1 adrenergic receptors!!!!
-brain arterioles LACK alpha 1 which is why we dont impact the brain! blood flow must be constant to the brain
where is the cardiovascular control center
medulla! integration center for blood pressure regulation
what does the hypothalamus do for vascular control
some control- blood flow to skin for temperature
what four hormones are involved in vascular control and what they do
(extrinsic)
- epinephrine and norepinephrine (norepinephrine-vasoconstriction/reinforce sympathetic . epinephrine- both vasoconstriction and vasodilation but preference for beta 2 vasodilation!! – the things that need it )
- vasopressin and angiotensin : fluid balance - impact blood pressure through water retention; slower acting
what organs for vaso control have beta 2 receptors
skeletal muscles and heart (and more)
what organs have alpha 1 and not beta 2
digestive organs and kidneys
what do vasopressin and angiotensin II do for vessels
they result in vasoconstriction
-vasopressin -> water retention. angiotensin 2 is part of renin angiotensin-aldosterone system and regulates salt balance (promotes salt conservation during urine formation)
-conservation of salt = water retention. the water retentive effect of these hormones causes increase in blood volume and an INCREASE in blood pressure!!!!!!!
`what impact does histamine have on blood vessels
DILATES arterioles!! pathologically
-does not NORMALLY participate in controlling blood flow
where is histamine stored
mast cells and basophils - released during injury and acts as a paracrine, promotes relaxation of arteriolar smooth muscle
what impacts INTRINSIC control
- heat/cold application (therapeutic)
- response to shear stress - compensates for changes in longitudinal force of blood flow
- myogenic responses to stretch (autoregulation)
- histamine release (injuries and allergic responses)
what impacts extrinsic control
- vasopressin – vasoconstrictor effect
- angiotensin II (salt/water retention)-vasoconstrictor effect
- epinephrine and norepinephrine
how do hydrophilic molecules pass the capillary wall
pores!! single layer of endothelium
how many precapillary sphincters are open for restin muscles
10%
–blood flows thru available cap beds or metarteriole (thoroughfare channel, anastome- passage)
how does bulk flow occur
at capillaryes; distribution of fluid between plasma and interstitial fluid
-through pores - fluid and electrolytes fusion of vesicles to form pores, between endothelial cells,
what increases diffusion (3 things)
- minimize distance for diffusion
- maximize surface area
- minimize blood flow velocity
what are features of capillary pores - what can pass, how big are they?
- fluid filled pores- permit SMALL WATER SOLUBLE SUBSTANCES
- present in most capillaries
- size varies between organs!!
- in the brain the endothelial cells are held by tight junction and there are No pores
-PROTEINS can sometimes pass in discontinous capillaries
what are the 3 types of capillaries
- continous : basement mem intact, tight junctions- proteins can sometimes pass
- sinusoid (discontinuous) : may haveINCOMPLETE BASEMENT MEMBRANE
- fenestrated : basement mem intact. some pores,some tight junctions
what is bulk flow important for
- protein free plasma filters out of capillary and mixes w interstitial fluid and reabsorbed - important for ECF distribution between interstitial fluid and plasma -
- HELPS MAINTAIN ARTERIAL BLOOD PRESSURE - keeps plasma volume constant.
- if plasma volume goes down, blood pressure goes down.
- dpends on ultrafiltration and reabsorption
what is ultrafiltration
responsible for bulk flow near the arterial end of capillary!! hydrostatic pressure imparted by heart drives fluid out of capillary mostly thru pores, while plasma proteins are retained within vessels- FILTRATION- protein free plasma
-as you go along capillaries, protein amount stays constant but fluid loss to interstitial fluid, so protein concentration increases
pressure inside cap is higher than inward driving pressure
what drives bulk flow at arterial side
ultrafiltration
-pressure inside capillary is greater than the inward driving pressure so it leaves (hydrostatic pressure)
what drives bulk flow at arterial side
osmotic pressure – reabsorption! (pressure inside cap is less than inward driving pressure)
what are the net results of capillary/interstitial fluid exchange
-how is it compensated for
net loss of fluid in the plasma and a net gain in the interstitial fluid!!
- ultrafiltration is about 11 mm hg at eginning of caps and reabsorption is like 9 mmm hg at end of caps
- comprensation = lymph vessels converge into lymphatic ducts- drains into subclavian veins
what is feature of lymphatic vessels
has free overlapping edges; create a one way valve like opening in the vessel wall
-forced to close valves by fluid pressure in lymph vessel
how does lymph move in lymphatic vessels
far from capillaries depends on smooth muscle in vessel wal to generate pressure to move it towards the heart. stretching of the lymphatic vessel stretches smooth muscles which stimulates smooth muscle contraction, increasing pressure and pushing lymph forward.
-contraction of skeletal muscles also aids movement of lymph. lymphatic valces found within vessel prevent the backflow of lymph as the vessels is squeezed by smooth or skeletal
lymph system function
- return filtered fluid that wasnt reabsorbed
- defense against disease
- transport of absorbed fat (from digestion- fatty partcles too large to get into the blood)
- return of filtered protein- small amount of plasma protein leave most capillaries during filtration cant be reabsorbed into capillary
what causes edema
edema= swelling due to excess interstitial fluid
- reduced concentration of plasma proteins
- increased permeability of capillary walls (high BP/hydrostatic or disease)
- increased venous pressure
- blockage of lymph vessels
what can cause a decrease in plasma protein (3 things)
- kidney disease: loss of plasma protein in urine
- liver disease: reduced synthesis of plasma proteins
- diet deficient in protein
(–> edema)
what causes blood to pool in capillaries
increaesd VENOUS pressure!! because flow is dependent on pressure gradient!! makes it harder for blood to flow out of capillaries and into veins
need a higher hydrostatic pressure to restore pressure gradient here (working against osmotic pressure- reabsorption of fluid is reduced??)
-can also cause edema bc it wont go into veins?
what happens with blockage of lymph vessels
edema can occur with lymph vessels blocked.
-net flow is usually to interstitial (as we know) so basically w blocked lymph we get fluid that cant return to the circulatory system. also plasma proteins usually go to lymph, so they are stuck too and that makes osmotic pressure where more fluid wants to go out. reduces reabsorption
what are the veins that capillaries drain into called
venules
how does connective tissue of veins compare to arteries
more collagen fibers, and less elastin fibers (less elastic)
how much blood does the vein system carry vs the rest of the cardio system
more than 60% at rest!!! big storage capacity aka it moves sloowww
what are feature of vein valves
large veins have them
- 2 to 3 cm intervals
- one way obv
- prevents back movement
what can it lead to when valves dont function? what happens with it?
varicose veins-swollen and twisted - blue (doesnt impact cardiac output) bc homeostatic effects can compensate by increasing total circulation volume.
complications: formation of clots and pain. legs w/prolonged sitting or standing
what is the skeletal muscle pump sequence for veins
skeletal muscle contraction -> venous compression -> increased venous pressure -> decreased venous capacity
what is the respiratory pump?
respiratory activity causes pressure in chest cavity (5 mm) hg less than atmospheric pressure
- external pressure within limbs and abdomen are normal
- –> this creates a pressure gradient where blood moves from lower veins to the chest – this promotes venous return!!!! helps w flow back to the heart
what is cardiac suction?
while the heart is resting during diastole, expansion of the ventricles creates a negative pressure- cardiac suction!! this gradient enhances venous return and allows passive flow of blood into the ventricles
how does sympathetic activity relate to venous return? whats the overall result on cardiac output?
symp stimulation produces venous vasoconstriction
- increased venous pressure causes a pressure gradient!!!
- this increases flow, and the change in resistance isnt significant
- diameter of venous lumen is really large so vasoconstriction increases pressure. increased venous return and increased cardiac output!!!
what two things does blood flow to any organ depend on
mean arterial pressure and degree of vasoconstriction..
how does the system compensate for arterioles of one organ dilating?
arterioles of another must constrict to maintain adequate pressure. and the adequate pressure will bring blood to vasodilated vessels
– but still there is an inadequate suppy of blood so there could be a situtaion where arterioles are dilated without adequate blood volume and bp goes down–> lightheadedness or fainting!
what receptors monitor mean arteriole pressure
baroreceptors
what is the baroreceptor reflex
-where is it?
short term mechanism- regulates cardiac output and total peripheral resistance
- in Carotid sinus!! sends signals to cardiovascular control center in the medulla
- alters activity of autonomic nervous system to return mean arterial pressure to normal
- like with orthostatic hypertension (laying in supine, blood pressure decreases and arterioles relax, volume of blood in veins increases- when go stand the vesels are still dilated and blood pressure is insufficient for required blood flow since vessels are dilated. etc, temporarily low o2 to brain…
how does the baroreceptor reflex react
carotid sinus continuously generates action potentials. the rate of firing set the standard fequency for baseline mean arterial pressure. as the mean arterial presure increases the frequency of action potentials increases above the normal frequency. this starts a signaling process which leads to dilation of arterioles to decrease blood pressure. in situtaion where mean arteril blod pressure decreases– the frequency fo action potentials geenerated by carotid sinus decreases and it signals arterioles to contract (sends signal to medulla cardiovascular control system)
what is normal systolic /diastolic
systolic: less than 120
diastolic: less than 80
what is elevated systolic / diastolic
systolic: 120-129
diastolic: less than 80
what is high blood pressure - STAGE 1 hypertension? systolic/diastolic
systolic: 130-139
diastolic: 80-89
what is high blood pressure STAGE 2 hypertension s/d
s; 140 or higher
d; 90 or higher
what is hypertensive crisis s/d
s; higher than 180
diastolic ; higher than 120
CONSULT DOCTOR NOW
what are the most common hypertensions
primary 90%
secondary -10%
how can reduced bloodflow to kidneys cause secondary hypertension
-reduced blood flow to kidneys -> increased blood volume to compensate for reduced renal blood flow. angiotensin II=vasoconstrictor ! and uptake of salt causes more water reabsorption..
how does pheochromocytoma cause secondary hypertension
this is an adrenal medullary tumor that secretes excessive epinephrine and norepinephrine.
-results in increaes in cardiac output and generalized peripheral vasoconstriction
what is primary hypertension? what causes it/what increases risk
unknown cause
genetic disposition- increases with obesity, stress, smokking and dietary habits
- defects in salt management by kidneys can also cause it.. genetic variations in angiotensinogen (precursor for angiotensin II)
- excessive salt intake (salt retains water- more blood volume)
- diets low in fruits and veggies, dairy (low K and ca)
what is the recommended sodium intake for anyone with high bp or at risk? everyone else?h
risk or high: 3.8 g nacl
everyone else - 5.8 g nacl
what are hypertension complications
- heart (increased workload, pump against increased resistance)
- damaged blood vessels
- congestive heart failure
- stroke
- heart attack
- renal failure
