Cardiovascular system - Beye Flashcards
What is the cardiovascular function of vessels?
- distribution of blood to meet metabolic demands
- enable exchange/ delivery of nutrients, wastes, hormones
- role in heat regulation
- essential for hemostasis (clotting)
- modulating inflammatory responses
What is the organization of the CV system?
- arteries carry blood away from the heart -> can become/ branch arterioles then capillaries
- capillaries is where exchange occurs -> capillaries reunite to form venules and then veins
- veins carry blood back to the heart
Describe where the highest and lowest blood pressure occur?
- highest pressure in arteries, lowest in veins -> high to low, blood will flow
- highest at systolic pressure = ~120
- lowest at diastolic pressure= ~80
- 120/80 = normal
How do blood pressure cuffs work?
If inflated above systolic pressure -> don’t hear anything = no blood flow
-> then slowly release -> pressure drops until reaches systolic pressure = blood starts to flow during artery opening, can hear turbulent flow because of partial opening - how you know you’ve reached systolic pressure
-> then flow becomes smooth (don’t hear anything = laminar flow)
-> artery will collapse again during diastole -> start to hear vessel sounds because blood flows in turbulent manner in partially collapsed vessel
How do you calculate mean arterial pressure?
MAP = diastolic + 1/3 (systolic - diastolic)
* systole is shorter than diastole, thus diastole has greater influence on MAP
What is the pressure like in the pulmonary cardiovascular system?
- pulmonary circulation is very low pressure
- systole pressure usually 20 or less
- not a lot of resistance
- no gravitation force against
- not much distance to go
What is the anatomy of a blood vessel?
- Outer layer = tunica adventitia. Fibrous connective tissue. Blood vessels, nerves, lymphatics.
- Middle layer = tunica media. Smooth muscle (innervated by SNS), elastin (stretching fiber), collagen. Where changes to blood flow can occur.
- Innermost layer = tunica intima. Endothelial cells.
- tunica means layer
- exception: capillaries only have the innermost layer
What is endothelium cross talk?
Critical for homeostasis
- possess many receptors (respond to signals)
- secrete vasoactive substances (influence activity of smooth muscles)
- also act as force sensors (know the pressure blood is under + whether laminar/ turbulent flow) -> can change structure, gene expression based on flow dynamics
Describe the structure, blood characteristics and purpose of arteries
Distribution vessels
Structure: large diameter, thin walls compared to diameter (1/4 wall), lots of elastic fibres -> easy to distend/ stretch -> get continous flow, comes in, arteries stretch, heart pumps blood, then you get recoil from the stretch so blood continues to flow even without heart
Blood characteristics: very high blood pressure, high blood flow, small drop in pressure (low resistance), high blood velocity (highest)
Purpose: “shock absorbers” -> absorb pulsatile wave (absorb energy)
What is atherosclerosis? List some examples.
An artery disease
- deposits occur already in first decade of life
- as it progresses, it can impede blood flow - usually due to rupture/ clot -> important organs don’t get blood
- consequences depend on artery: coronary artery disease = heart attack/damage, cerebrovascular disease = stroke, peripheral artery disease = leg pains, muscles don’t get appropriate flow)
- in innermost layer, get build-up of cholesterol -> then white blood cells come in, try to phagocytose the cholesterol, become bigger and become foam cells -> can die and cholesterol is deposited -> cholesterol can harden to form calcium deposits
Describe the structure, blood characteristics and purpose of arterioles
Resistance vessels
Structure: small diameter, thick walls compared to diameter (50% of lumen diameter), lots of smooth muscle -> SNS
Blood characteristics: large drop in pressure (compared to arteries), slower blood velocity
Purpose: controls blood flow (vasoconstriction, vasodilation)
What is the relationship between pressure, blood flow and resistance?
- blood flows down a pressure gradient (high to low)
- but resistance decreases flow
Blood flow = P1 - P2 or
Blood flow = pressure gradient/ resistance
How do you calculate resistance?
resistance = (8Ln) / (pi r^4)
Where, L= length of the vessel, n= viscosity of the fluid, r= radius of the vessel
Describe the structure, blood characteristics and purpose of veins
Capacitance vessels
Structure: large diameter (larger than arteries), very thin walls compared to diameter (10% of lumen diameter), some elastic fibers and smooth muscle -> SNS innervates smooth muscle (can undergo vasoconstriction/dilation), contain valves to prevent backflow
Blood characteristics: very low blood pressure, medium blood velocity
Purpose: “blood reserve” -> 70% of all systemic blood is in our veins, ability to store blood, can increase venous return (maximize) because there is so much
What is the relationship between blood velocity and total cross-sectional area? What is the significance?
- more total cross-sectional area = slower flow
- slower flow = maximize exchange
- capillaries = most cross sectional area because there are so many - this influences blood velocity
- velocity (speed) does not equal flow (total amount)
What are varicose veins?
- backflow of blood, presses on wall, stretches veins
- happens in superficial veins (can see them)
- valve and elastin failures
- can be painful
- genetically predisposed
- obesity and smoking predispose
- not dangerous -> still have deep veins that can return blood
- spider veins are a type of varicose veins, seen in 50% of people
- can have them surgically removed
Why do we need to regulate blood flow?
- to increase blood supply to active tissues and decrease it to inactive tissues
- to maintain blood supply to vital organs - heart and brain at all times
- to maintain blood pressure (MAP)
- to increase or decrease heat loss from the body by redistributing blood
What is Hagen-Poiseuille’s equation?
Blood flow = (pressure gradient* pi* r^4) / (8 L n)
How can you change blood viscosity?
- blood doping: take blood out then add all back right before competition, get more red blood cells - more oxygen (e.g. Lance Armstrong), carry more oxygen to muscle cells - good for sports. Erythropoietin (peptide hormone) acts on bone marrow to increase red blood cell production - blood doping increases erythropoiesis -> increases blood viscosity, increases resistance to flow, heart has to work harder
- dehydration -> decreased plasma volume -> increased viscosity
- body temperature -> higher temp. small decrease in visocisty (body temp highly regulated, don’t see huge changes = small changes in viscosity
Describe vasoconstriction
Increases resistance thus decreases flow
-> decrease radius, decrease bloodflow, increase resistance
Describe vasodilation
Decreases resistance thus increases flow
-> increase radius, increases bloodflow, decreases resistance
What are the mechanisms used to regulate blood flow?
- Local (intrinsic) -> tissue environment (temp, gases, pressure)
- Humoral (extrinsic) -> substances in blood (e.g. hormones, inflammatory mediators, paracrine factors)
- Neural (extrinsic) -> nervous system, autonomic
Describe the local (intrinsic) mechanism used to regulate blood flow
Autoregulatory mechanisms (tissue itself regulates blood flow - no nervous system input)
1. Myogenic derived -> involves smooth muscle stretch (muscle derived)
2. Metabolic derived -> involves matching metabolic needs (metabolic needs of the tissue)
What is the myogenic theory?
Sudden increase in blood pressure -> this stretches walls of arterioles -> triggers opening of stretch-sensitive cation channels -> smooth muscle in arteriole walls contracts (reduce radius) -> decreases blood flow and pressure AFTER constriction
*this protects and maintains normal blood flow
What is the metabolic theory?
Change metabolism, change metabolites, and tissue conditions
- increases CO2
- decreases O2 (use more, levels decrease)
- increases H+ proton concentration = decrease in pH (lactic acid - use of muscles)
- increase in adenosine from ATP breakdown
- increase in K+ ECF (APs can cause this)
- increase in temperature (start to sweat when in motion)
*these conditions cause arterioles to vasodilate to increase flow = vasodilator metabolites (VDM’s) = means more flow
What is hyperemia
Increased flow (from vasodilation)
- increased VDM’s (act on arterioles, can’t act on capillaries don’t have smooth muslce, don’t change radius)
- vasodilation
* get reactive hyperemia after have a blood pressure cuff on
Why might someone pass out after hyperventilating?
- higher oxygen
- higher pH
- lower CO2
- opposite of hyperemia
-> vasoconstriction = drop in flow, blood vessels to brain vasoconstrict, why you pass out
How do you calculate cardiac output (whole body)?
Cardiac output (CO) = mean arterial pressure (MAP) / total peripheral resistance (TPR)
* this is comparable to the blood flow equation which = pressure gradient / resistance
What are some common vasoconstrictors?
- Antidiuretic hormone
- Angiotensin II
- Epinephrine
- Endothelin-1 -> can be released in blood and act on neighbouring smooth muscle cells, substance made by endothelial cells, important for normal tone/state of vessels (GPCR receptor)
- Some prostaglandins (thromboxane A2) - almost all your tissues produce paracrine factors, some cause vasoconstriction, some cause vasodilation (GPCR receptor)
Describe antidiuretic hormone (ADH)
- a peptide hormone released from posterior pituitary (neuron - neuro hormone)
- also known as vasopressin (pressor = increased pressure)
- stimulus: decrease in MAP (+ other stimuli)
- binds to V1a receptor (GPCR) on vascular smooth muscle (target tissue)
- ADH clamps down on vessels- increases pressure, increase MAP
Describe angiotensin II
- a peptide hormone produced in the blood (pre cursor released in liver)
- stimulus: decrease in MAP (+ other stimuli)
- binds to AT1 receptor (GPCR) on vascular smooth muscle
- produced by series of reactions (cleave proteins)
What are some common vasodilators?
- Atrial natriuretic peptide (ANP)
- Bradykinin and histamine
- Epinephrine
- Nitric oxide (released by endothelial cells, paracrine - act local, causes smooth muscle relaxation from release of cyclic GMP)
- Some prostaglandins (prostacyclin) - act to relax smooth muscle
Describe atrial natriuretic peptide (ANP)
- a peptide hormone released from atrial myocytes (released by the heart, from muscle cells in atrium)
- stimulus: increase in MAP
- binds to NPR-A (natriuretic peptide receptor, a membrane guanylyl cyclase receptor -> increases presence of cyclic GMP)
- decreases pressure by opening up vessels
Describe bradykinin and histamine
- inflammatory mediators
- binds endothelial or smooth muscle receptors (complex mechanism)
- causes major drop in blood pressure
- can be caused by anaphylaxis
Describe epinephrine and its the complex response
- an amine hormone, released from adrenal gland (also called adrenaline, circulates in blood)
- stimulus: SNS stimulation
- binds to adrenergic receptors (alpha and beta) - GPCRs -> alpha = vasoconstriction (Gq + phospholipase, release of Ca+), beta = vasodilation
1. Vasoconstriction -> binds to alpha adrenergic receptors (found in almost all tissues) - Gq, (found in GI tract, kidney, others)
2. Vasodilation -> binds to beta2 adrenergic receptors (found in arterioles of the following tissues: lungs, coronary vessels, skeletal muscle, liver) - consider in fight or flight, what is constricted and what is dilated
Describe the neural (extrinsic) mechanism used to regulate blood flow
Autonomic nervous system
- sympathetic nervous system
- parasympathetic nervous system
Describe the sympathetic nervous system (SNS) mechanism of regulating blood flow
Neural (extrinsic) mechanism
-> innervates smooth muscle in arterioles (increase TPR)
-> innervates smooth muscle in veins (venous return -> increases EDV) (increases SV)
-> innervates SA and AV node, ventricular muscle (increases HR)
e.g. norepinephrine
Describe the parasympathetic nervous system (PNS) mechanism of regulating blood flow
Neural (extrinsic) mechanism
-> no vascular smooth muscle innervation (does not communicate, no direct impact on blood vessel)
-> indirect effects because no SNS activation
-> innervates SA and AV node - alters blood pressure through cardiac output effects, myocardium to minor extent
Describe the baroreceptor reflex
Set point: MAP -> control centre: CV centre in medulla -> (SNS and PSNS) -> effector: heart and blood vessels -> controlled variable: MAP -> sensors: baroreceptors (mechanoreceptors) -> (A.P.) -> back to control centre
- Reflex activation =
-> MAP decreases: increase via SNS activation
-> MAP increases: decrease via PSNS activation
Describe arterial baroreceptors
- located in walls of aortic arch, carotid sinuses
- mechanoreceptors -> stretch sensitive (lead to depolarization)
- monitor MAP
- send action potentials to cardiovascular centre in medulla oblongata
Describe the cardiovascular centre: medulla oblongata
- nucleus ambiguus (NAc): excitatory connection -> PSNS
- Rostral ventrolateral medulla (RVLM): inhibitory connection -> SNS
- more activity of NTS = more activation of PSNS + inhibition of SNS
- less activity of NTS = less activation of PSNS + less inhibition of SNS
NTS = nucleus tractus solitarius (NTS), barosensitive neurons
What occurs when mean arterial pressure is too low (MAP)?
Less stretch in aorta, carotid sinus = less baroreceptor activity -> decreased frequency of action potentials to NTS -> less excitement of NAc, less inhibition of RVLM -> less PSNS outflow, more SNS outflow -> increases heart rate, increases stroke volume, increases cardiac output
What is orthostatic hypotension?
- affects 6% of population, increases with age
- defined as decrease in systolic (>20 mmHg) and diastolic pressures (>10 mmHg) within 3 minutes of standing (MAP drops more than normal, pooling in lower extremities, not returning to heart/ brain
- symptoms: light-headed, dizzy, blurred vision, others (when standing up - gravity causes pooling)
- multiple causes: drugs, e.g. antihypertensives acting on SNS, neurogenic causes - ANS impairment, neurodegenerative disease, idiopathic -> genetic component
What are the factors at play for the cardiovascular system in exercise?
- intensity and duration
- age
- fitness level (heart rate might be higher with lower fitness level)
- type: dynamic or static
