BIO 313 exam 2 lecture

overview of arteries/capillaries/veins

arteries: carry blood away from the heart, most of the time carry oxygenated blood

capillaries: smallest of blood vessels for nutrient and gas exchange

veins: carry blood to the heart, most of the time carry deoxygenated blood

structure of blood vessels

tunica interna: simple squamous epithelium, endothelium

tunica media: smooth muscle

tunica externa: connective tissue

arteries

• elastic contractile walls

• contraction maintains blood pressure

• elasticity allows for expansions due to blood pumping out of heart

• vasoconstriction: contraction of smooth muscle, decreases diameter

• vasodilation: relaxation of smooth muscle, increases diameter

elastic arteries

• conducting arteries

• transport large volumes of blood away from the heart

• tunica media: lots of elastic fiber, tolerate huge pressure differential

• they can minimize blood pressure by minimizing pressure peaks

muscular arteries

• distribution arteries

• distribute blood to muscles and organs

• tunica media more muscular, often times “pressure points“

capillaries

• only vessels that permit exchange, due to thin walls they decrease diffusion distance, due to relatively slow moving blood

• tunica interna: 1 cell later thick, endothelium, gas and nutrient exchange

continuous capillaries

• most places in body

• single endothelial cell=full circumference

• bound together by tight junctions

• permit diffusion of water, small solutes, lipid and soluble materials

• prevent diffusion of blood cells and plasma proteins

fenestrated capillaries

• windows/porous

• permit rapid exchange of water and solutes, small peptides

• found in places for absorption or filtration like kidneys and choroid plexus

sinusoidal capillaries

• very specialized

• permit free exchange

• bone marrow

• spleen, phagocytes stick cytoplasmic extensions through to monitor RBCs

capillary beds

• interconnected network of capillaries

• may receive from more than one artery (collaterals)

• 1 arteriole gives rise to lots of capillaries

• blood flow regulated by precapillary sphincters

• vasomotion: constant control of blood entering into capillary beds, controlled by local changes like oxygen

venous circulation

• venules: collect blood from capillary beds and are smallest venous vessels

• veins: capacitance vessels, store blood

• low bp=thinner walls

• cannot overcome gravity, contain valves to prevent back flow

• most of blood distribution is from systemic veins, capillaries arteries and heart are a lot less

blood vessel physiology

• purpose of CV regulation is to maintain flow

• blood flow= cardiac output (under ideal conditions)

• increasing cardiac output increases blood flow to capillaries

• flow= change in pressure/resistance

• pressure decreases as it gets further from the heart

flow through tubes

Flow=change in pressure/resistance

resistance is determined by length, viscosity, and radius

what increases length is increase in size, more BV increase in viscosity is increase in EPO or dehydration, increase in radius is from different receptors for different signaling molecules.

• radius is easiest to change and has biggest effect bc its raised to the 4th power

• a change in pressure as long as its the same across 2 tubes is identical and therefore doesnt change the rate of blood flow

flow through cardiovascular system

near the heart the pressure is high for vessels, but the further it gets from the heart the less pressure there is, and the smaller the arteries/veins the less pressure: high pressure near aorta, low pressure in capillary beds and veins: mean arterial pressure

• systemic has a lot higher pressure than pulmonary

• sum of resistance in all vessels is total peripheral resistance, flow rate can be measured with cardiac output

arteries

receive blood from heart

• great arteries have a lot of elasticity so they enlarge when blood is pumped into them, if you lose elasticity heart has to pump harder

• allows them to hold a lot of blood at a reasonable pressure

• pressure variations in vessels depends on cyclic change or change associated through different types of vessels

arterial blood pressure

• maintains blood flow through capillaries, has to be higher than peripheral resistance

• peak pressure in arteries during ventricular systole=systolic pressure (elevated systolic pressure can dislodge clots and damage vessels)

• peak pressure in arteries during ventricular diastole=diastolic pressure

  • pulse pressure= systole-diastole

  • mean arterial pressure: diastolic+1/3 (pulse pressure)

  • both pulse pressure and MAP decrease the further from the heart

pressures in vascular system

• response to pulsing of the heart, the pulses of pressure move throughout vasculature decreasing in amplitude with distance

• arteries are pressure reservoir, they stretch when they receive blood from aorta and then their elasticity squeezes blood moving it

• decreased elasticity of BV with aging leads to increased MAP, this is needed to be able to push the blood to all of the body because elasticity has less role

arterioles

resistance vessels

• decrease their diameter: increasing resistance or increasing BP

smallest arteries

poorly defined tunica externa

tunica media: 1-2 layers

changes in diameter due to hormonal or nervous stimulation: through NE, E, or innervation

• they are the resistance vessels so they control the arteriolar radius since that has the biggest affect on flow (length and viscosity are still there)

• through relaxation and contraction in their smooth muscle they can determine which organs get more blood or less blood which is important for fight/slight, rest/digest

blood flow to individual organs

• flow to the organ depends on MAP/resistance, and because MAP is identical through body flow to a specific organ depends on the resistance offered by arterioles of each organ

• example: exercise blood flow has an increase in skeletal muscle, a decrease in digestive organs, and an increase in heart. this results from vasoconstriction or vasodilation

local controls

active hyperemia: working out

exercising muscle→ a decrease in O2, increase in CO2, increase in H+, increase in other metabolic factors in ecf→ vasodilation of arterioles (overrides extrinsic sympathetic input) → increase muscle blood flow (active hyperemia)

flow auto regulation: depends on intrinsic factors in organs

decrease in arterial pressure in organ→ decrease in blood flow to organ→ decrease in O2, increase in metabolites, decrease vessel wall stretch in organ→ arteriolar dilation in organ→ restoration of blood flow toward normal in organ

• both provoke vasodilation through local signals

intrinsic versus extrinsic control of arteriolar smooth muscle

vasodilation:

intrinsic control (autoregulation): metabolic or myogenic controls that distribute blood to organs and tissues, metabolic: decrease O2, increase CO2/H+, increase K+; prostaglandins, adenosine, nitric oxide myogenic: less stretch from decrease in bp

extrinsic control: neural/hormonal changes, maintain MAP, redistribute blood during exercise and thermoregulation; decrease sympathetic tone (neural), atrial natriuretic peptide (hormonal)

vasoconstriction

intrinsic: myogenic- stretch, metabolic- endothelins

extrinsic: neural, increase sympathetic tone, hormona- angiotensin II, antidiuretic hormone, epinephrine, norepinephrine

increase in MAP

increase in cardiac output through increase SV/ HR

increase peripheral resistance through decrease diameter of BV, increase blood viscosity, increase vessel length

regulation

tissue perfusion

• blood flow through the tissues

• regulation ensures blood flows, occurs at appropriate times, occurs in right areas, without drastically changing pressures to vital organs

mechanisms of regulation

short term regulation: neural mechanisms, endocrine mechanisms

long term regulation: renal mechanisms

autoregulation: chemical changes in ISF, causes immediate localized adjustments

neural mechanisms

centers responsible for global change

• cardiac centers

  • sympathetic (cardioacceleatory) and parasympathetic (cardioinhibitory) influence the heart

• vasomotor centers: vasoconstriction neurons (adrenergic NE) or vasodilator neurons (skeletal muscle/brain vessels, nitrous oxide, cholinergic neurons activate nitric oxide release, acetylcholine)

monitoring of arterial blood

baroreceptor reflexes: monitor degree of stretch in organ walls

• carotid sinus, aortic sinus, right atrial wall

adjust cardiac output and resistance to maintain arterial pressure

hemostasis in blood vessels

1. stimulus: increase in blood pressure/ decrease in blood pressure

2. baroreceptors in carotid sinus and aortic arch are stimulated/inhibited

3. increase or decrease impulse from baroreceptors to stimulate cardioinhibitory center and inhibit cardioaccelatory center+inhibit vasomotor center, or stimulate vasomotor, activate cardioaccelatory, inhibit cardioinhibitory

4. a- decrease sympathetic impulses to the heart, decrease HR, contractility and CO, or increase sympathetic activity to heart increasing those

4. b- decrease rate of vasomotor impulses, alowing vasodilation by decreasing R, or vasomotor fibers stimulate vasoconstriction causing increase in R

5. decrease in CO and R to return blood to hemostatic range, or increase

chemoreceptors and hormonal mechanisms

chemo: respond to changes in CO2, oxygen, or PH levels

located in carotid and aortic bodies and medulla oblongata

activate cardioaccelatory, inhibit cardioinhibitory

hormonal: provides short term and long term affects

direct and indirect increase in MAP

direct:

decrease in arterial pressure, decrease in filtration in kidneys, decrease in urine, increase in blood volume, increase in MAP

indirect:

uses renin, angiotesin, aldosterone

decrease in arterial pressure, baroreceptors detect change (can relate to homeostatic figure), increase in sympathetic activity, kidney releases renin

renin converts angiotesinogen (made in liver, in circulation) to angiotesin I, then ACE or angiotesin converting enzyme converts that to angiotesin II

causes 4 things

1. vasoconstriction by increasing peripheral resistance, which increase MAP

2. increase in thirst (hypothalamus) which increase water intake increasing blood volume increasing MAP

3. increasing antidiuretic hormone, decreases urination so more water reabsorption, increasing blood volume, increasing MAP

4. adrenal cortex uses aldosterone to increase Na reabsorption in the kidneys, keeping more sodium in regulation, urinate less

overview of increase in MAP

increase in body size increases length of BV, increase in hematocrit increases blood viscosity; E, NE, antidiuretic hormone, and angiotesin II increase vasomotor tone which all decrease radius, these lead to increase peripheral resistance which increases MAP

crisis stressors lead to increase in CO2, decrease in O2, increase in H changing the pH which is detected by chemoreceptors and sensed in vasomotor centers for cardioaccelatory

fluid loss leads to decrease BV and pressure, sensed by baroreceptors, also sensed in vasomotor centers for cardioacceleration

• both can lead to increase HR increase SV increase CO increase MAP

decrease atrial natriuretic hormone, increase in sodium and water conservation, increase in blood volume, increase in EDV by venous return

increase activity of respiratory centers and musclular pumps increases EDV by venous return which do the same with SV HR

3 controls of arteriolar smooth muscle

neural controls

• vasoconstrictors: sympathetic nerves

• vasodilators: neurons that release nitric oxide

hormonal controls

• vasoconstrictiors: E, vasopressin (antidiuretic), angiotesin II

• vasodilators: E, atrial natriuretic hormone

local controls:

• vasoconstrictors: internal BP (myogenic response), endothelin

• vasodilators: decrease o2, increase in K, co2, H, osmolarity, adenosine, bradykinin, nitric oxide, substances released during injury

effects of hormones on BP

E/NE: increase CO (HR and contractility) with beta 1 receptors in heart, increase peripheral resistance in arterioles with alpha 1 receptors

angiotensin II: increase PR in arterioles

atrial natriuretic peptide: decrease PR in arterioles

antidiuretic hormone: increase PR in arterioles, increase BV in kidney

aldosterone: increase BV in kidney

autoregulation

local vasodilation: decreased tissue oxygen, lactic acids, NO, increase K or H, inflammation chemicals, elevated local temperature

local vasoconstriction: prostaglandins, thromboxanes, endothelins

extrinsic factors controlling arterioles

• serve whole body

• sympathetic nerves supply mainly arterioles, NE generally causes vasoconstriction through alpha adrenergic receptors

• nitric oxide is a vasodilator and is released by some nonadrenergic autonomic neurons (affects sexual organs)

• hormones: angiotensin II, vasopressin both cause vasoconstriction, atrial natriuretic factor is a vasodilator, epinephrine can cause vasodilation (binding to beta receptor) or vasoconstriction (binding to alpha receptor)

stimulation of receptors

• sympathetic postganglionic neurons to skeletal muscle arterioles, release norepinephrine which increase NE in ECF, alpha receptor to smooth muscle in skeletal muscle arterioles. vasoconstriction averts blood away from that location

• adrenal medulla secretes E into blood, increase plasma E, binds to either alpha or beta receptor, if binds to beta then theres vasodilation and more blood flow.

bulk flow

determines relative fluid volumes in the blood stream and interstitial space

• movement of fluids and solutes out is called filtration, movement in is reabsorption

• ECF contains 3L plasma and 10L interstitial fluid which has slow movement

• movement of blood in capillaries is slower because it goes into a bunch of branches but volume moved per unit is equal

• as the number of capillary tubes in the beds goes up, the movement of blood slows down: adequate time and surface area for exchange between capillary blood and ISF

• precapillary sphincters manage capillary blood flow, when open they allow blood to all of bed, when closed blood only flows through the main channel, they are regulated by extrinsic and local factors

capillary filtration

removal of solutes as a solution flows across porous membrane or fenestrated capillary

4 types

1. diffusion through membrane (lipid soluble (o2))

2. movement through intracellular clefts (water soluble)

3. movement through fenestrations (larger water soluble)

4. transport via vesicles or caveloae (large substances)

filtration and reabsorption

• bulk fluid flow causes continuous mixing of plasma and ISF maintaining interstitial environment

• hydrostatic pressure: pushes, blood pressure

• osmotic pressure: sucks, due to blood proteins, albumin

capillary hydrostatic pressure HPc: capillary blood pressure forcing fluid out of capillary walls, arterial 35mmhg and venous 17mmhg

interstitial fluid hydrostatic pressure HPif: pressure pushing fluids back into vessel, zero because lymphatic vessels drain ISF

capillary osmotic pressure or oncotic pressure OPc: sucking of albumin proteins pulling water into capillary, 26mmhg, doesn’t change between veins/arteries

interstitial fluid osmotic pressure: OPif: interstitial fluid has low protein content so about 1

• net filtration pressure (NFP): (HPc+OPif)-(HPif+OPc), net fluid out is filtration (+10) net fluid in is reabsorption (-8)

• more fluid leaves at arterial end than returned at venous end bc excess ISF is returned to blood via lymphatic system

• net filtration and reabsorption balance meaning no net fluid movement

hemostatic imbalances in blood pressure

hypertension=chronically elevated blood pressure due to high CO or high R, most of the time is due to high resistance especially with age

• normal BP is 120/80 or slightly lower, high blood pressure is anywhere from 130+/80+

• no cure but can be controlled with lifestyle changes like weight loss(length), and drinking more water (viscosity), resistance is the easiest to change with medications that allow vasodilation (ACE inhibitors, diuretics to increase urine output and decrease bv)

hypotension: low blood pressure (below 90/60), due to underlying condition or being tall

• orthostatic hypotension is common in older adults

• sensors in carotid and aorta dont respond to falling bp, heart fails to beat faster to compensate, blood pools in veins in lower body due to gravity

shock

circulatory shock: blood vessels are inadequately filled with blood and blood doesn’t circulate normally

hypovolemic shock: large blood/fluid loss

vascular shock: poor circulation due to extreme vasodilation; anaphylaxis, bacterial infection, ANS dysfunction

cardiogenic shock: pump failure

when hemostasis fails

blood volume loss→ inadequate tissue perfusion (low o2 and nutrients to cells), cells metabolize anaerobically (without o2) lactic acid buildup, water leaves tissue cells moves into blood and cells dehydrate

• body will try to do normal mechanisms to increase MAP and increase BP

• if fluid volume continues to decrease blood pressure drops, a drop in blood pressure os a late sign

• the goal of all responses is to maintain blood pressure

• signs that it’s too late include tachycardia leading to clammy and cold skin, restlessness (early sing), coma (late sign), reduced oxygen to brain leading to passing out

venous pressure

low, determines venous return (impacts cardiac output by EDV)

effective pressure is 16mmhg

at rest most of blood volume is in veins (capacitance vessels)

• factors affecting venous pressure

• muscular pump: contractions of muscle around veins

• respiratory pump: inhalation decreases pressure in pleural cavity ad pulls blood into inferior vena cava, exhalation increases pressure in cavity and pushed blood into right atrium

• sympathetic venoconstriction: smooth muscle in veins under sympathetic control

alterations in venous return

• alter end diastolic volume which increases SV and CO

• increase in blood volume, increase in inspiration movements, increase in sk muscle pump, increase in activity of sympathetic nerves to veins

• all increase venous pressure, increasing venous return, increasing arterial pressure, increasing EDV, increasing SV

• more going in=more going out

lymphatic system

• vessels pick up fluid in tissues like lg molecules, insoluble lipids, bacterial toxins

• lymph nodes house many wbcs and serve as a trigger for immune system

• lymph fluid is the mismatch between absorption and filtration in capillaries

• returns to the blood in the veins, major reentry point is subclavian veins which dump into right atrium

• lymph flow to heart: one way valves, compression from tissues, myogenic response (contraction) in larger vessels

  • pressure on the outside of the vessel pushes the endothelial cells edge inwards which allows entrance of ISF (lymph)

  • high pressure inside the valve forces edges to overlap so lymph can’t escape

functions of the respiratory system

Acid base balance: influences pH of body fluids by eliminating CO2

blood pressure regulation: assists with synthesis of angiotensin II, a hormone that regulated blood pressure

blood and lymph flow: breathing creates pressure gradients between thorax and abdomen that promote flow of lymph and blood

blood filtration: lungs filter small clots

communication: speech and other vocalizations

gas exchange: o2 and co2 exchanged between blood and air

platelet production: more than half of platelets are made by megakaryocytes in lungs

olfaction: smell

four processes of respiration

respiratory system

1. pulmonary ventilation (breathing): movement of air into and out of lungs

2. external respiration: exchange of o2 and co2 between lungs and blood

circulatory system

3. transport of o2 and co2 in blood

4. internal respiration: echange of o2 and co2 between systemic blood vessels and tissues

upper versus lower respiratory system

upper: nose (air), mouth (air/food), pharynx or throat (air/food) with trachea and esophagus

lower: trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alvelopar ducts, alveolar sacs, lungs

conducting versus respiratory zones

conducting zones: trachea, bronchi, bronchioles, terminal bronchioles (air transport)

respiratory zones: respiratory bronchioles, alveolar ducts, alveolar sacs. where respiration occurs (gas exchange between lungs and blood), doesn’t work without conducting zones

respiratory mucosa

mucous membrane

• lines conducting portions

• contains epithelium and underlying supportive connective tissue

  • ciliated psudestratified columnar epithelium in nasal cavity, pharynx, upper part of lower respiratory system: trap bacteria+mucous elevator

  • stratified squamous in lower pharynx: protects against friction

  • stratified cuboidal in smaller bronchioles: structural support and protection

  • simple squamous in alveoli for gas exchange bc thin layer

mucociliary elevator

• reduces chances of bacterial infection in respiratory zone

• cilia move in one direction and push mucus towards mouth out of lungs, out of trachea and into esophagus where it goes into stomach

• smoking damages cilia, produces excess mucus making it thicker, inhaled debris and dust/pathogens get trapped

• cystic fibrosis makes it hard for cilia to move because mucus is so thick, bacteria gets trapped bc cilia cant sweep it out as well

respiratory membrane

• pulmonary capillaries that surround alveolar sacs that form respiratory membrane with alveoli

• pressure is lower in the lungs because if it was high it could blow them out

• air fills alveolar spaces and gas exchange occurs through respiratory membrane, it includes a fused basement membrane

  • epithelial cells: simple squamous alveolar cells

  • endothelial cells: lining capillaries

  • basal lamina: between alveolar and endothelial cells (all epithelial cells are supported by CT), it’s very thin for easy transport

  • macrophages for defense

  • type II alveolar cells secrete surfactant in the water film coating inside of alveolar sacs, it allows lungs to expand when wet

pleura

visceral pleura, parietal pleura, and the pleural cavity holding pleural fluid

• surface tension of the pleural fluid resists separation of the two pleura so they don’t rub together, you wan’t surface tension so it clings to the larger cavity otherwise they collapse

lung volumes and capacities

atmospheric pressure: from the air that we are breathing in, is 0mmhg

intrapleural pressure: pressure within the pleural cavity, it is from the elastic recoil of the lungs balanced by the elastic expansion of the thoracic wall, it has to be negative, -4mmhg. if the recoil is more powerful the lungs will want to collapse and expel ari, if the expansion is more powerful the lungs will want to spring out and draw air in

intrapulmonary pressure (alveolar pressure): changes from the expansion and relaxation of the lungs, it balances with atmospheric pressure and it has to be 0

transpulmonary pressure: this is the difference between intrapulmonary and intrapleural pressures, it has to be positive 4 to balance them to 0: it dictates whether the lungs expand or recoil, altering the volume and pressure within intrapulmonary or the alveloi

lung volumes interacting

inhalation: intrapleural pressure becomes more negative as you breathe in because the visceral pleura is pulled further than it wants to be, transpulmonary pressure also increases to match the difference in this pressure, which means there’s an increase in the expansion of the lungs, however intrapulmonary pressure decreases only slightly pulling air into the lungs

exhalation: lungs experience elastic recoil of the visceral pulling inward, the intrapleural pressure becomes less negative, transpulmonary pressure decreases back to normal, and the intrapulmonary pressure becomes slightly positive causing air to flow out of the lungs

boyle’s law

airflow= change in pressure/resistance, difference in atmospheric pressure and alveoli divided by airflow resistance

as you inhale, the volume of your lungs expands, the pressure within your lungs decreases and this moves air in

as you exhale, the volume of your lungs decreases, the pressure within them increases and this causes air movement out

• we change the volume in order to change the pressure

• intrapulmonary pressure determines the direction of airflow in the respiratory tract and intrapleural pressure has to always remain negative.

transpulmonary pressure will always be maintained while intrapulmonary and intraplueral change, the increase in volume decreases pressure, the decrease in volume increases pressure

quiet inhalation and forced inhalation

1. inspiratory muscles get shorter to contract (diaphragm descends and rib cage rises, external intercostals contract)

2. thoracic cavity volume increases

3. lungs are stretched which increases intrapulmonary volume

4. intrapulmonary pressure drops to -1

5. air flows into lungs down pressure gradient until intrapulmonary pressure is equal to atmospheric pressure (0)

forced inhalation: uses accessory muscles like sternocleidomastoid, scalenes, pectoralis and they are recruited for a slight increase in volume leading to a decrease in pressure and more air flowing in

• asthma

quiet exhalation and forced exhalation

1. inspiratory muscles relax (diaphragm rises, rib cage and sternum are depressed from relaxation of external intercostal)

2. thoracic cavity volume decreases

3. elastic lungs recoil passively and intrapulmonary volume decreases

4. intrapulmonary pressure rises to +1

5. air flows out of lungs down pressure gradient until intrapulmonary pressure is 0

forceful exhaling or active breathing: uses internal intercostals to pull down ribs, and abdomen to pull down ribs the volume decreases the pressure increases and it causes you to exhale air.

• getting punched in the gut

when transpulmonary pressure is not positive

• the lungs collapse

pneumothorax makes intrapulmonary pressure= intrapleural pressure meaning there is no difference in transpulmonary pressure

• traumatic pneumothorax is from a puncture in the wounds from getting stabbed

• spontaneous pneumothorax is from a hold in the lungs

• if you have a wound in one lung you can still have the second lung that functions normally