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Human Physiology > Cardiovascular system - Beye > Flashcards

Cardiovascular system - Beye Flashcards

1
Q

What is the cardiovascular function of vessels?

A
  1. distribution of blood to meet metabolic demands
  2. enable exchange/ delivery of nutrients, wastes, hormones
  3. role in heat regulation
  4. essential for hemostasis (clotting)
  5. modulating inflammatory responses
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2
Q

What is the organization of the CV system?

A
  • 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
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3
Q

Describe where the highest and lowest blood pressure occur?

A
  • 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
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4
Q

How do blood pressure cuffs work?

A

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

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5
Q

How do you calculate mean arterial pressure?

A

MAP = diastolic + 1/3 (systolic - diastolic)
* systole is shorter than diastole, thus diastole has greater influence on MAP

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6
Q

What is the pressure like in the pulmonary cardiovascular system?

A
  • 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
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7
Q

What is the anatomy of a blood vessel?

A
  • 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
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8
Q

What is endothelium cross talk?

A

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

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9
Q

Describe the structure, blood characteristics and purpose of arteries

A

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)

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10
Q

What is atherosclerosis? List some examples.

A

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

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11
Q

Describe the structure, blood characteristics and purpose of arterioles

A

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)

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12
Q

What is the relationship between pressure, blood flow and resistance?

A
  • blood flows down a pressure gradient (high to low)
  • but resistance decreases flow
    Blood flow = P1 - P2 or
    Blood flow = pressure gradient/ resistance
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13
Q

How do you calculate resistance?

A

resistance = (8Ln) / (pi r^4)
Where, L= length of the vessel, n= viscosity of the fluid, r= radius of the vessel

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14
Q

Describe the structure, blood characteristics and purpose of veins

A

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

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15
Q

What is the relationship between blood velocity and total cross-sectional area? What is the significance?

A
  • 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)
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16
Q

What are varicose veins?

A
  • 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
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17
Q

Why do we need to regulate blood flow?

A
  • 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
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18
Q

What is Hagen-Poiseuille’s equation?

A

Blood flow = (pressure gradient* pi* r^4) / (8 L n)

19
Q

How can you change blood viscosity?

A
  • 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
20
Q

Describe vasoconstriction

A

Increases resistance thus decreases flow
-> decrease radius, decrease bloodflow, increase resistance

21
Q

Describe vasodilation

A

Decreases resistance thus increases flow
-> increase radius, increases bloodflow, decreases resistance

22
Q

What are the mechanisms used to regulate blood flow?

A
  1. Local (intrinsic) -> tissue environment (temp, gases, pressure)
  2. Humoral (extrinsic) -> substances in blood (e.g. hormones, inflammatory mediators, paracrine factors)
  3. Neural (extrinsic) -> nervous system, autonomic
23
Q

Describe the local (intrinsic) mechanism used to regulate blood flow

A

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)

24
Q

What is the myogenic theory?

A

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

25
Q

What is the metabolic theory?

A

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

26
Q

What is hyperemia

A

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

27
Q

Why might someone pass out after hyperventilating?

A
  • higher oxygen
  • higher pH
  • lower CO2
  • opposite of hyperemia
    -> vasoconstriction = drop in flow, blood vessels to brain vasoconstrict, why you pass out
28
Q

How do you calculate cardiac output (whole body)?

A

Cardiac output (CO) = mean arterial pressure (MAP) / total peripheral resistance (TPR)
* this is comparable to the blood flow equation which = pressure gradient / resistance

29
Q

What are some common vasoconstrictors?

A
  1. Antidiuretic hormone
  2. Angiotensin II
  3. Epinephrine
  4. 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)
  5. Some prostaglandins (thromboxane A2) - almost all your tissues produce paracrine factors, some cause vasoconstriction, some cause vasodilation (GPCR receptor)
30
Q

Describe antidiuretic hormone (ADH)

A
  • 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
31
Q

Describe angiotensin II

A
  • 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)
32
Q

What are some common vasodilators?

A
  1. Atrial natriuretic peptide (ANP)
  2. Bradykinin and histamine
  3. Epinephrine
  4. Nitric oxide (released by endothelial cells, paracrine - act local, causes smooth muscle relaxation from release of cyclic GMP)
  5. Some prostaglandins (prostacyclin) - act to relax smooth muscle
33
Q

Describe atrial natriuretic peptide (ANP)

A
  • 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
34
Q

Describe bradykinin and histamine

A
  • inflammatory mediators
  • binds endothelial or smooth muscle receptors (complex mechanism)
  • causes major drop in blood pressure
  • can be caused by anaphylaxis
35
Q

Describe epinephrine and its the complex response

A
  • 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
36
Q

Describe the neural (extrinsic) mechanism used to regulate blood flow

A

Autonomic nervous system
- sympathetic nervous system
- parasympathetic nervous system

37
Q

Describe the sympathetic nervous system (SNS) mechanism of regulating blood flow

A

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

38
Q

Describe the parasympathetic nervous system (PNS) mechanism of regulating blood flow

A

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

39
Q

Describe the baroreceptor reflex

A

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

40
Q

Describe arterial baroreceptors

A
  • 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
41
Q

Describe the cardiovascular centre: medulla oblongata

A
  • 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
42
Q

What occurs when mean arterial pressure is too low (MAP)?

A

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

43
Q

What is orthostatic hypotension?

A
  • 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
44
Q

What are the factors at play for the cardiovascular system in exercise?

A
  • intensity and duration
  • age
  • fitness level (heart rate might be higher with lower fitness level)
  • type: dynamic or static

Human Physiology (13 decks)

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