Vasculature Flashcards
What governs vascular resistance?
Vessel length + internal vessel radius: determines surface area in contact with blood
blood viscosity: friction between molecules of a flowing fluid and proprotional to hematocrit
What determines hemodynamics?
1) pressure differences between two points in the cardiovascular system
2) vascular resistance impeding blood flow
What does poiseuille’s law state about the relationship between flow, resistance and radius?
Resistance and radius are INVERSELY proporrtional
Resistance and flow are INVERSELY proportional
Flow and Radius are DIRECTLY proportional.
What are the layers of the artery from lumen and out?
- Tunica Interna: inner single layer of specialized endothelial cells continuous with endocaridium
- Elastica Interna: inner layer of stretchable elastin fibres
- Tunica Media: thick layer of smooth muscle whose contraction and relaxation alters vessel radius
- Elastica Externa: outer layer of elastin
- Tunica Externa: sheath of tough collagen surrounding vessel to prevent overstretching.
What are arteries?
thick walled elastic vessels that act as rapid transit passageways between heart and organs, and provide a pressure reservoire.
What does the arterial pressure reservoire do?
Maintains a driving force for blood flow during diastole and a constant flow of blood to the capillaries.
How does the pressure reservoire maintain a constant and driving force for blood flow?
- Semilunar valve opens and blood is ejected from ventricle in systole.
- Aorta expands to hold excess volume of ejected blood, which holds potential energy.
- Semilunar valve closes due to pressure of aorta in diastole.
- Passive elastic recoil releases potential energy as kinetic energy and returns to original shape, the narrowing of walls pushing excess blood downstream.
What are artieries?
thin vessels with little elastic tissue and lots of smooth muscle rechly innervated by sympathetic nerves that act as as resistance vessels of the body.
What are the 3 important functions of arteries?
- determine the relative blood flow to indvidual tissues/organs
- help regulate mean arteriole pressure
- Eliminate pulse pressure prior to it reaching the capillaries
How do arterioles adjust flow rate to their organs?
- Radius of arterioles at different parts of the body vasodilate/contstrict independently from one another
- Precapillary sphincters relax/constrict to open up access to the capillary bed or close off the bed and redirect through a metarteriole.
How is vasodilation and vasoconstriction modulated in arterioles?
Smooth muscle is in a state of partial contraction (vascular tone) independent of neural/chemical input, but altered by external signals that decrease or increase smooth muscle’s [Ca++]
What is the difference between intrinsic and extrinsic autoregulation of blood vessel caliber?
Intrinsic: Signals are local factors (metabolic, myogenic) that come from and control individual tissues/organs to match metabolic needs
Extrinsic: Signals originate outside the local tissue, typically from the nervous system or endocrine system and control to maintain homeostasis BP
What are the three mechanisms of intrinsic autoregulation?
Myogenic control: responds to changes in mean arterial pressure
Local metabolic control: metabolically driven release of paracrine agents
Non metabolic chemical mediators: endothelin-1, histamine, serotonin
How does myogenic control of blood vessels work during increase in BP, very low BP, and very high BP?
Increase in blood pressure: stretch of arteriole opens mechanically gated Ca++ channels, inducing constriction via Ca induced Ca release in smooth muscle
Very low blood pressure: lack of blood results in emptier vessels, inducing passive collapse
Very high blood pressure: excess blood results in excess filling of vessels, inducing passive dilation
How does metabolic control take part in blood vessel autoregulation?
Rapidly contracting muscle leads to local hypoxia and local increase in CO2 (cellular respiration), H+ (lactic acid fermentation), K+ (rapid consecutive depolarizations) and adenosine (precursor to ATP). This induces NO release from vascular endothelium.
What is NO’s role in autoregulation?
[NO] reduces Ca2+ entry into adjacent smooth muscle, inducing localized vasodilation of arterioles and precapillary sphincters.
What is the difference between active hyperemia and reactive hyperemia?
Active hyperemia: increase in blood flow to tissues in response to metabolic demands from increase in activity
Reactive hyperemia: increase in blood flow to tissues following period of low blood flow sensed by diminished stretch (induces relaxation) and localized hypoxia/metabolic byproduct accumulation (induces vasodilation)
How does endothelin-1 act as a non-metabolic chemical mediator?
Vasoconstrictor released by arteriolar endothelium that opens non-stretch sensitive Ca++ channels, inducing Ca induced Ca release
How does histamine act as a non-metabolic chemical mediator?
From Mast cells: vasodilator released during allergic reactions (quick onset)
From Basophils: vasodilator released during injury or infection (2-8 hr onset)
How does serotonin act as a non-metabolic chemical mediator?
Released within platelets in the blood upon sensing a wound, which activates release and induces vasoconstriction to lower blood flow at the site of the injury.
How do sympathetic neurons control arteriolar radius?
Sympathetic neurons in the medulla oblongata tonically release NE to arteriolar SM a1-adrenergic receptors. Increased firing causes vasoconstriction superimposed on basal tone, and decreased firing leads to vasodilation.
How do hormones control arteriolar radius primarily?
Sympathetically induced epinephrine release from adrenal glands bind to SM a1-receptors, reinforcing vasoconstriction.
However heart, liver, and skeletal muscle arteriolar SM membranes predominantly have B2-adrenergic receptors that bind to epinephrine with a higher affinity, resulting in dilation.
What are other hormones other than epinephrine involved in extrinsic regulation of blood vessel diameter?
atrial natriuretic peptide, vaspressin, angiotensin II, angiotensin 1-7
How is atrial natriuretic peptide (ANP) released and involved in regulation of blood vessel diameter?
Formation: Atria stretch due to increased pressure and volume from preload, which causes specialized cells in atria to synthesize ANP.
Purpose: It causes vascular SM relaxation (lowers resistance, increases flow) and encourages kidneys to excrete water and Na+ (decreases blood volume)
How is vasopressin released and involved in regulation of blood vessel diameter?
Formation: Released by posterior pituitary in response to decrease in blood volume/MAP sensed in atrial receptors.
Purpose: It acts as a vasoconstrictor (to maintain BP), as well as an antidiuretic promoting water conservation (increases blood volume)
How is angiotensin II formed and involved in regulation of blood vessel diameter?
Formation: Low perfusion pressure in kindeys triggers release of renin which converts angiotensinogen to angiotensin I which is converted to angiotensin II in the blood.
Purpose: Angiotensin II acts as a vasoconstrictor and causes the kidneys to retain sodium and water, which increases blood volume and blood pressure.
What is a severe hemorrhage’s effect on the body?
- loss of blood causes MAP to decrease
- decreases arteriolar stretch, decreasing flow
- decreased O2 and increased metabolite at capillary beds due to lack of flow
What is the concurrent systemic response of the body against a severe hemorrhage?
- Sympathetic stimulation releases norepinephrine causing vasoconstriction of SM in non-essential organs
- Sympathetic stimulation induces epinephrine release from adrenal medulla binding to a1-receptors inducing constriction in non essential areas, as well as b2-receptors inducing dilation in skeletal muscle
- increased plasma vasopressin and angiotensin II (conservation of water and Na+ via kidneys)
How is angiotensin 1-7 involved in regulation of blood vessel diameter?
Formation: cleavage of angiotensin II by epithelium localized angiotensin converting enzyme 2 (ACE2)
Purpose: Binds to GPCR that initiates a signalling pathway that produces nitric oxide
What is the effect of COVID-19 on ACE2?
SARS-CoV-2 binds to ACE2, localized in epithelium of cardiovascular, respiratory, renal and digestive systems. SARS-CoV-2/ACE2 binding prevents ACE2 from binding to GPCR and acting as a vasodilator, as well as allows SARS-CoV-2 into the tissue.
What are capillaries?
Smallest, thinnest, and most numerous blood vessels in the body acting as the primary site for cardiovascular exchange.
What are the parts of a capillary?
- single layer of epithelial cells encased by glycoprotein/collagen matrix (basal lamina)
- Intercellular pores/junctions (continuous capillaries)
- Fenestrations (fenestrated capillaries)
What is able to pass through Intracellular pores/junctions, and what is able to pass through the endothelial cell lipid membrane?
pores/junctions: small, water-soluble substances (H2O, Na+, K+, glucose, amino acids)
passive diffusion: O2, CO2, fatty acids, steroid hormones, anesthetics
How are proteins exchanged in the capillaries?
Transcytosis: Proteins are actively transported via ATPase mediated endocytosis into the epithelial cells, and then out of the cells into the tissues via ATPase mediated exocytosis.
What is the purpose of moving material across capillary walls?
- exchange of material between blood and nearby cells via concentration, pressure, and electrochemical gradients
- maintaining fluid balance between plasma and interstitial fluid via absorption and filtration by Starling forces
What are starling forces?
Hydrostatic pressure and colloid osmotic pressure that drives the bulk flow of plasma into and out of capillaries to regulate plasma and interstitial fluid balance.
What are the 4 starling forces?
- Capillary hydrostatic pressure (Pc)
- Interstitial fluid hydrostatic pressure (Pi)
- Plasma colloid-osmotic pressure (πc)
- Interstitial fluid colloid-osmotic pressure (πi)
What is the capillary hydrostatic pressure (Pc)?
Capillary hydrostatic pressure (Pc) is the pressure that favours filtration of plasma OUT of the capillary. It declines from the arteriole (~37mmHg) to the venule side (~15mmHg)
Why does the capillary hydrostatic pressure decline as blood moves from the arteriole to the venule side?
- Narrowness of capillary results in increased resistance which creates friction and lowers pressure.
- Loss of plasma from capillary due to filtration reduces blood volume, which lower pressure
What is interstitial hydrostatic pressure?
Interstitial hydrostatic pressure Pi is the pressure outisde the capillary favouring absorption of interstitial fluid INTO the capillary due to concentration gradient. (1mmHg)
What is net filtration pressure (Net P)?
Force favouring plasma filtration along the entire length of the capillary. Pc-Pi at any given point along the capillary.
What ist he plasma colloid osmotic pressure?
Osmotic pressure within the capillary due to nonpermeating solutes, that favour the absorption of interstitial fluid INTO the capillary. (25mmHg)
What is the Interstitial fluid colloid osmotic pressure?
Osmotic pressure due to non penetrating solutes withtin the ISF that favours plasma filtration OUT of the capillary. (0mmHg)
What is the net colloid-osmotic pressure? (Net π)
force favouring absorption of ISF along the entire length of the capillary. πc-πi at any given point along the capillary
What is the lymphatic system?
A system of vessels surrounding the cardiovascular system that allows excess interstitial fluid to enter, that drain into the blood stream via ducts near the jugular veins.
What is edema and what is it caused by?
Accumulation of interstitial fluid within tissues caused by obstruction of lymph vessels, increase in Net P or decrease in Net π
What are two ways lymph vessels are obstructed in a manner that causes edema?
a) elephantiasis from mosquito-borne filaria worms
b) removal of lymph nodes
How does an increase in Net P create edema?
Increased Net P from heart failure promotes venous pooling, backing blood up into the capillaries, which increases increase Pc
How does a decrease in Net π result in an edema?
- Liver disease: decreased plasma protein production changes osmotic gradient, reducing reabsorption of interstitial fluid into the capillaries
- Kidney disease: increased protein excretion reduces protein content in blood, changing osmotic gradient and reducing reabsorption of interstitial fluid into the capillaries.
What is histamine’s role in creating edema?
- dilates arterioles which allows more blood to flow into capillaries, which increases Pc
- increases intercellular pore size, increasing capillary permeability for proteins, increasing πi (osmotic gradient favouring exit from capillary)
What are veins/venules structure and function?
Structure: thin walled, one way valved, oval lumen vessel with low SM and elastin, but high collagen
Function: low resistance conduits for blood flow back into the heart. volume reservoire
What is the mean driving pressure for blood flow from peripheral veins to the right atrium?
10-15mmHg, increases with volume
How are veins blood volume reservoires?
Hold a much greater volume of blood than arteries, even though pressure is much lower, and can be rapidly drawn upon when required (exercise)
What is the result of gravity acting on blood and lymph vessel columns?
Below heart level, veins and lymph vessels fill and be distended, leading to edema (from pushback into capillaries) and eventually fainting.
What is venous return influenced by?
neural input, skeletal muscle pump, respiratory pump, cardiac suction
How is venous return influenced by neural input?
Walls of veins contain SM innervated by sympathetic neurons, releasing norepi which binds to a1-adrenergic receptors, inducing vasoconstriction which increases venous pressure and resistance.
How does skeletal muscle influence venous return?
Large muscle groups compress deep veins during contraction, which squeeze veins, pumping the blood out the one way valves.
How does the respiratory system influence venous return?
Inspiriation, chest wall expansion and diaphragm descension causes decrease in thoracic pressure and increase in abdominal pressure.
Distension of thoracic veins (pulling open) due to vaccuum, allows more blood to enter the veins to return to the atrium.
Compression of abdominal veins drives blood to lower pressure areas towards the right atrium.
How does cardiac suction act as a pump?
Ventricular systole pulls atrial floor down, decreasing atrial pressure, promoting venous return. During diastole, elastic potential is released and causes a suction force that sucks blood from atria into ventricles.
What is the magnitude of cardiac suction dependent on?
Magnitude of suction effect is dependent on end systolic volume, as the less volume, the faster the ventricles are filled.
How does the short term regulation of MAP work?
Mechanical stretch receptors (baroreceptors) in aortic arch and carotid sinuses detect changes in blood/pulse pressure. These nerves project to cardiovascular control center in medulla and autonomic adjusting firing to effectors.
How does the carotid sinus nerve impulses, vagus nerve impulses, sympathetic cardiac nerve impulses, sympathetic vasoconstrictor nerve impulses, respond to LOW pulse pressure?
Carotid sinus nerve impulses: decrease firing due to sensing less stretch on carotid sinus and aortic arch
Vagus nerve: fire AP less to prevent ACh release and allows sympathetic nervous system to dominate and increase heart rate
Sympathetic cardiac nerve impulses: Fire AP more to release more NE at the heart and increase heart rate and contractility
Sympathetic vasoconstrictor nerve impules: Fire AP more to cause vasoconstriction, raising MAP
How does the carotid sinus nerve impulses, vagus nerve impulses, sympathetic cardiac nerve impulses, sympathetic vasoconstrictor nerve impulses, respond to HIGH pulse pressure?
carotid sinus nerve impulses: increase firing due to sensing of stretch at aortic arch and carotid sinus
Vagus nerve impulses: increase firing to release ACh and allow parasympathetic system to dominate
Sympathetic cardiac nerve impulses: decreases firing to release less NE to slow heart rate and decrease contractility
Sympathetic vasoconstrictor nerve impulses: decreases firing to release less NE to decrease vascular diameter
How does the long term regulation of MAP work?
Blood volume is regulated by hormones secreted by the heart, brain and kidneys that influence fluid intake and urine output (e.g. ANP, vasopressin, renin and angiotensin II)
How does atrial natriuretic peptide affect MAP?
- increases Na+ and H2O excretion by kidneys (increasing urine output)
- Inhibits vasopressin secretion (dilates vasculature)
- Inhibits renin secretion (inhibits production of angiotensin II which inhibits constriction)
What is hyper tension?
Consistent BP 140/90 and MAP > 100mmHg generally due to a chronic increase in total peripheral resistance
What is the difference between primary and secondary hypertension?
Primary: associated with obesity, stress, high cholesterol, smoking, genetics, Na+ retention and immune system responses leading to hypertrophy of the left ventricle and diminishing of contractile function.
Secondary: increase in mean arterial pressure due to other conditions (e.g. in pregnancy, the placenta increases levels of angiotensin II, increasing vasoconstrction and increasing BP)
What are treatments for primary hypertension?
a) exercise, decreased Na+ intake, weight loss to lower resting MAP
b) Ca2+ channel blockers to promote vasodilation in heart and bloodvessels, reducing Ca++ release and decreases heart contractility and heart rate
c) diuretics to increase urinary excretion of Na+ and H2O
d) beta adrenergic receptor blockers to decrease NE and E release, inhibiting stimulation of cardiac output
e) angiotensin-converting enzyme inhibitors to block production of angiotensin II and decrease TPR
